Description	Reaction	Enzymes	Disease Name
Up-regulation of ADAR1 may be suppressing the ADAR2 function and results in hypo-editing in PDE8A1 gene transcripts of SLE T cells.	A:I		Systemic Lupus Erythematosus
A general decrease in editing activity of the human BLCAP transcript in cancerous tissues	A:I	ADAR ADARB1	Astrocytoma
Alu-dependent A-to-I RNA editing increases in rheumatoid arthritis. Cathepsin S and TNF receptor-associated factors 1,2,3 and 5 are among the hyper-edited transcripts	A:I	ADAR	Rheumatoid Arthritis
Mutations of the ADAR may impair its tertiary structure, entailing its defective activity, and are linked to the onset of DSH.	A:I	ADAR	Dyschromatosis Symmetrica Hereditaria
The genes related to migration and cytoskeleton are the target of m1A modification. This epigenetic chaneg cause poor overall survival.	A:m1A	ALKBH3	Hodgkin lymphoma
In patient cells, a functional NSUN2 protein is lacking. NSUN2-depletion causes growth retardation, mild microcephaly, and learning disabilities.	C:m5C	NSUN2	Dubowitz-like Syndrome
Hypermethylation of 4506 in 28S subunit of the ribosome leads to ribosome biogenesis deregulation	N:Nm	FBL NOP58	β-thalassemia
NSUN2 and YBX1 stabilize the oncogene mRNA of the oncogene HDGF that mediates UCB pathogenesis in human	C:m5C	NSUN2 YBX1	Urothelial carcinoma of the bladder (UCB)
Associations between the FTO SNPs and type 2 diabetes,  further investigation is needed to identify the causal genetic variants and potential mechanisms underlying the observed genetic associations	A:m6A	FTO	Type 2 Diabetes
RNA editing, on different transcripts, promotes the disease risk and is closely associated with type 2 Diabetes	A:I	ADARB1	Type 2 Diabetes
METTL3 and METTL14 protein levels are decreased in whole islets from T2D patients. the Insulin/IGF1 -AKT-PDX1 pathway is significantly affected by hypomethylation in T2D	A:m6A	METTL14 METTL3	Type 2 Diabetes
Inhibition of the production of properly modified leading to impaired proliferation and differentiation of specific embryonic cells. Downregulated expression of treacle resulted in decrease 2'-O-Me of 18S pre-rRNA	N:Nm	NOP56 TCOF1	Treacher Collins syndrome
Pseudouridylation level on snRNA U2 depends on expression level of scaRNA1that is linked with TOF	U:Y	PUS7	Tetralogy of Fallot (TOF)
Increased C-to-U RNA editing mediated by APOBEC1 leads to neuronal gain-of-function through presynaptic activity of RNA-edited GlyRs, resulting in facilitation of neurotransmitter release	C:U	APOBEC1	Temporal Lobe Epilepsy
The degree of R/G editing is significantly increased in the hippocampal tissue and in neo-cortical tissue in patients	A:I	ADARB1	Temporal Lobe Epilepsy
The reduced editing at the R/G site of glutamate receptor subunits (GluRs) is likely to reduce post-synaptic excitatory responses to glutamate, thus duce post-synaptic excitatory responses to glutamate, thus limiting the progression of cell death.	A:I	ADARB1	Spinal Cord Injury
RNA editing in GluR-B is essential for brain development to avoid the alteration of calcium permeability which affects mice seizure and survival	A:I	ADARB1	Severe epilepsy
RNA editing of A3A induces changes in WT1 mRNA which correspond to driver cancer mutations suggests a potential role for this novel modification in cancer mutagenesis	C:U	APOBEC3A	Wilms tumor and
m6A methylation (induced by METTL3) protects against RCCs proliferation, migration and invasion functions , and EMT and PI3K-Akt-mTOR pathways may be involved in the potential mechanisms.	A:m6A	METTL3	Renal cell carcinoma
Increased P2RX6 mRNA m6A methylation level (induced by METTL14) enhances P2RX6 pre-mRNA splicing, decreases ATP-P2RX6-Ca2+ −p-ERK1/2-MMP9 axis and protects against RCCs migration and invasion.	A:m6A	METTL14	Renal cell carcinoma
Demethylation of adenosine residues in the 3′‐UTR of PGC‐1α mRNA (induced by FTO), leads to increased PGC‐1α mRNA stability and protein expression, and increased mitochondrial biogenesis, oxidative stress and tumour suppression	A:m6A	FTO	Renal cell carcinoma
In RCC cell lines and tissues, WTAP is significantly overexpressed. Mechanistic studies exhibited that CDK2 expression is positively associated with the expression of WTAP. Moreover, WTAP stabilizes CDK2 transcript to enhance CDK2 expression via binding to 3′-UTR of CDK2 transcript.	A:m6A	WTAP	Renal cell carcinoma
RNA editing inhibits the enzymatic activity of TPH2 splice variants	C:U	ADARB1	Psychiatric disorders
5HT2C editing is altered in individuals suffering from psychiatric disorders	A:I	ADARB1	Psychiatric disorders
5HT2C editing is altered in individuals suffering from psychiatric disorders	A:I		Psychiatric disorders
Alteration in 5HTR2C RNA editing levels in the brain of suicides	A:I	ADARB1	Psychiatric disorders
YTHDF2 is the direct target of miR-493-3p and it is frequently upregulated in both PCa tissues and cell lines. Instead, miR-493-3p is downregulated. The overexpression of YTHDF2 and inhibition of miR-493-3p reduce m6A levels and increase the proliferation and migration of cancer cells	A:m6A	YTHDF2	Prostate cancer
METTL3 is overexpressed in prostate cancer cell lines, together with increased m6A content. SHH-GLI signaling positively correlates with the severity of PC and METTL3 regulates the expression level of GLI1	A:m6A	METTL3	Prostate cancer
m6A levels of POI patients is increased and FTO gene expression and protein levels are decreased. Thus, FTO could increase the risk of complications of POI	A:m6A	FTO	Premature ovarian insufficiency
The overexpression of FTO reduces m6A levels and increases NMDAR1 expression levels, NMDAR1, which could elevate oxidative stress and Ca2+. High expression of NMDAR1 will damage neurons and cause subsequent apoptotic death	A:m6A	FTO	Parkinson
RNA editing repairs the PINK1 W437amber mutation rescue the PINK1/Parkin-mediated mitophagy	A:I	ADARB1	Parkinson
m6A methylation is regulating apoptosis and chemo/radioresistance. Methylation of METTL3 target genes is inducing a decrease in apoptotic responses to GEM and it is also protecting from DNA damage after UVC.	A:m6A	METTL3	Pancreatic cancer
YTHDF2 binds to m6A-containing mRNAs and regulates their localization and stability. YTHDF2 upregulation increases the proliferative abilities of pancreatic cells by enhancing Akt/GSK3b/CyclinD1 pathway and on the opposite side it represses the invasion and migration abilities (EMT) by supressing the YAP pathway	A:m6A	YTHDF2	Pancreatic cancer
YTHDF2 binds to m6A-containing mRNAs and regulates their localization and stability. YTHDF2 upregulation increases the proliferative abilities of pancreatic cells by enhancing Akt/GSK3b/CyclinD1 pathway and on the opposite side it represses the invasion and migration abilities (EMT) by supressing the YAP pathway	A:m6A	YTHDF2	Pancreatic cancer
A CNV-containing DNA region (which contains YTHDC2 gene) is found to be associated to pancreatic cancer risk	A:m6A	YTHDC2	Pancreatic cancer
Increased KCNK15-AS1 lncRNA m6A methylation level is negatively correlated with KCNK15-AS1 expression and it sustains the proliferation, invasion and migration of pancreatic cancer cells. Decreased expression of ALKBH5 in pancreatic cancer cell determines an increased methylation of KCNK15-AS1 lncRNA, a decreased KCNK15-AS1 expression and an increased proliferation, migration and invasion of pancreatic cancer cells.	A:m6A	ALKBH5	Pancreatic cancer
ALKBH5 decreases WIF-1 mRNA m6A levels and thus increases WIF protein levels. The upregulation of WIF-1 inhibits Wnt pathway and its downstream targets, leading to the inhibition of pancreatic tumorigenesis and sensitization to chemotherapy. Thus, the downregulation of ALKBH5 in pancreatic cancer, induces PDAC cell proliferation, migration, invasion, tumorigenesis, and metastasis in vitro and in vivo.	A:m6A	ALKBH5	Pancreatic cancer
Nsun6 was found to be an important factor that enables supress the pancreatic cancer cell proliferation	C:m5C	NSUN6	Pancreatic cancer
CSF-1 expression is increased by the overexpression of ALKBH3. This results in cancer cell invasiveness without affecting cell proliferation and migration	A:m1A	ALKBH3	Ovarian and breast cancer
Expression level of METTL3 are up-regulated in human OS tissues and OS cell lines. METTL3 promotes osteosarcoma cell progression by regulating the m6A level of LEF1 and activating Wnt/b-catenin signaling pathway.	A:m6A	METTL3	Osteosarcoma
Decreased m6A level in bone marrow mesenchymal stem cells (MSCs) induces pathological features of osteoporosis in mice (impaired bone formation, incompetent osteogenic differentiation potential, and increased marrow adiposity). PTH (parathyroid hormone)/Pth1r (parathyroid hormone receptor-1) signaling axis is an important downstream pathway for m6A regulation in MSCs. METTL3 loss of function reduces the translation efficiency of MSCs lineage allocator Pth1r and disrupts the PTH-induced osteogenic and adipogenic responses in vivo.	A:m6A	METTL3	Osteoporosis
Association between FTO SNPs and higher obesity risk, but further investigation is warranted to identify the causal genetic variants and potential mechanisms underlying the observed genetic associations	A:m6A	FTO	Obesity
2’-O-methylation of tRNAPhe may impact the development.	N:Nm	FTSJ1	Nonsyndromic X-Linked Intellectual Disability
METTL3 promotes the translation of oncogenes such as EGFR and TAZ independently from its catalytic activity and m6A readers. The expression of these oncogenes mediates NSCLC cells growth, survival and invasion. METTL3 upregulation is reached by the downregulaion of miR-33a in NSCLC cells which normally reduces the expression of METTL3 by targeting its 3'UTR region.	A:m6A	METTL3	Non-small cell lung cancer
Direct physical and functional interaction between METTL3 and the eukaryotic translation initiation factor 3 subunit h (eIF3h). The METTL3–eIF3h interaction is required for enhanced translation (BRD4), formation of densely packed polyribosomes and oncogenic transformation.	A:m6A	METTL3	Non-small cell lung cancer
METTL3 is overexpressed in lung cancer tissues and cell lines. The m6A mRNA methylation initiated by METTL3 promotes YAP mRNA translation via recruiting YTHDF1/3 and eIF3b to the translation initiation complex and increases YAP mRNA stability through regulating the MALAT1-miR-1914-3p- YAP axis. The increased YAP expression and activity induce NSCLC drug resistance and metastasis.	A:m6A	METTL3	Non-small cell lung cancer
miR-143-3p is upregulated in the paired BM tissues as compared with that in primary cancer tissues. m6A methyltransferase Mettl3 can increase the splicing of precursor miR-143-3p to facilitate its biogenesis. It targets the three binding sites of 3’UTR of vasohibin-1 (VASH1) to inhibit its expression. Mechanistically, VASH1 can increase the ubiquitylation of VEGFA to trigger the proteasome mediated degradation, further, it can endow the tubulin depolymerization through detyrosination to increase the cell motility. Thus, miR-143-3p by inhibiting VASH1 t can increase the invasion capability and angiogenesis of lung cancer	A:m6A	METTL3	Non-small cell lung cancer
Increased m6A methylation level reduces USP7 mRNA expression and reduces both the proliferation rate of lung cancer cells and the capacity of colony formation. The increased USP7 mRNA stability through FTO mediated demethylation explaines FTO oncogenic role for the growth of NSCLC cells	A:m6A	FTO	Non-small cell lung cancer
Increased m6A methylation level reduces MZF1 mRNA expression. FTO upregulation mediates MZF1 mRNA demethylation and increased MZF1 mRNA stability. This leads to an enhanced MZF1 expression, which explains the oncogenic roles of FTO in LUSCs	A:m6A	FTO	Non-small cell lung cancer
YTHDF2 is upregulated in lung cancer tissues and it recognizes m6A sites on the 3′UTR of 6-phosphogluconate dehydrogenase(6PGD) and facilitates its translation, which advances the pentose phosphate pathway (PPP) flux , which is crucial for tumor growth.	A:m6A	YTHDF2	Non-small cell lung cancer
Intermittent hipoxia (HI) promotes the expression of ALKBH5 in lung adenocarcinoma. The m6A demethylase ALKBH5 affects the proliferation and invasion of lung adenocarcinoma cells under IH by downregulating m6A modification on FOXM1 mRNA and by promoting FOXM1 expression. FOXM1 has been reported to play an important role in cell proliferation, cell cycle, cell differentiation, angiogenesis and metastasis, and also with cisplatin-based chemotherapy resistance	A:m6A	ALKBH5	Non-small cell lung cancer
ALKBH5 is upregulated in the NSCLC tissue and cells. ALKBH5 induces the demethylation of TIMP3 transcript to repress its mRNA stability leading to NSCLC tumor progression	A:m6A	ALKBH5	Non-small cell lung cancer
C→U editing of NF1 RNA creates a translational stop codon, potentially leading to premature truncation of neurofibromin	C:U	APOBEC1	Neurofibromatosis
C→U editing of NF1 RNA creates a translational stop codon, potentially leading to premature truncation of neurofibromin	C:U	APOBEC1	Neurofibromatosis
Loss of m5C causes the accumulation of tRNA fragments in the absence of NSUN2. Therefore, reduction in protein translation rates and activation in stress pathways leading to reduced cell size and increased apoptosis of cortical, hippocampal, and striatal neurons occurred.	C:m5C	NSUN2	Neuro-developmental disorder
Ψ modification in the CUG repeats induces structural stabilization, prevents MBNL1 binding, and rescues mis-splicing	U:Y		Myotonic dystrophy type 2 (DM2)
Missing m1A modification on mitochondrial tRNA at the 58 position is associated with the MERRF disease. m1A58 provides a positive charge on tRNA tertiary structure that affect the binding of elongation factor which delivers tRNA to ribosome.	A:m1A	Trmt61B	Myoclonus epilepsy, ragged-red fibers (MERRF)
Deregulation GLI1 RNA editing is correlated to multiple myeloma	A:I	ADAR	Myeloma
Mutation in PUS1 gene affects an amino acid, that cause a defect in pseudouridylation. Deficient pseudouridylation of mitochondrial tRNAs has been associated to MLASA	U:Y	Pus1	Mitochondrial myopathy and sideroblastic anemia (MLASA)
LAck of modifications in mitochondrial and cytoplasmic tRNAs from MLASA patients at sites normally modified by Pus1p.	U:Y	Pus1	Mitochondrial myopathy and sideroblastic anemia (MLASA)
DKC1 encodes dykerin which can induce the pseudoridylation of rRNA. Defects in the pseudouridylation activity of dyskerin is related to the development of malignancy in patients with DC	U:Y	DKC1	Metachronous rectal adenocarcinomas with dyskeratosis congenita (DC)
The increased m6A methylation level, in melanoma-promoting genes, PD-1 (PDCD1), CXCR4, and SOX10, promotes melanoma cells proliferation, migration and invasion in vitro and melanoma tumor growth in vivo. FTO was found to be upregulated in melanoma, suggesting a protumorigenic role. FTO higher expression is induced by metabolic stress and starvation. It was found that PD-1 (PDCD1), CXCR4, and SOX10 are regulated by FTO-mediated demethylation which blocks the YTHDF2-induced mRNA decay (tumor suppressor). Furthermore, FTO-mediated demethylation plays an important role in therapeutic resistance to anti-PD-1 immunotherapy and cell killing by IFNγ	A:m6A	FTO	Melanoma
Increased m6A methylation level (due to METTL3 upregulation) promotes melanoma cell lines colony formation and invasion. MMP2 and N-cadherin play a crucial role in invasion and metastasis of melanoma cells and their expression was found to be associated to METTL3 upregulation. These results indicate that METTL3 may regulate MMP2 and N-cadherin. Whereas MMP2 expression depends on the catalytic activity of METTL3, regulation of N-cadherin appears to be independent of METTL3 catalytic activity.	A:m6A	METTL3	Melanoma
Decreased m6A levels are identified in ocular melanoma samples, indicating poor prognosis, and changes in global m6A modification are highly associated with tumor progression. Mechanistically, YTHDF1 promotes the translation of methylated mRNA of HINT2, a tumor suppressor in ocular melanoma.	A:m6A	YTHDF1	Melanoma
The association between MPM and asbestos exposure is established but the mechanism is unclear. It was proposed that asbestos causes DNA damage by inducing DNA alkylation and methylation. Thus, methylation could be at the bases of the MPM onset and the characterized FTO rs9939609 polymorphism which alters its expression level, may play a role in asbestos-induced methylation and carcinogenesis	A:m6A	FTO	Malignant pleural mesothelioma
rs12936694 from the m6A demethylase gene ALKBH5 showed allelic and genotypic association to major depressive disorder	A:m6A	ALKBH5	Major depressive disorder
Association between SNP rs9939609 within FTO and major depressive disorder, independently from BMI	A:m6A	FTO	Major depressive disorder
Significant increase in m5C in circulating tumor cells of lung cancer.	C:m5C		Lung cancer
ADAR1 gene amplification is oncogenic in lung cancer and can enhance cell growth and invasion	A:I	ADAR	Lung cancer
Loss of 2'-O-Me results in decreased leukemia self-renewal potential and reduced colony formation potential.	N:Nm	DDX21 FBL TLE5	Leukemia
Reduced levels of METTL3/METTL14 may lead to pathogenesis and progression of E/R-positive acute lymphoblastic leukemia and increase relapse rates.	A:m6A	METTL14 METTL3	Leukemia
Mutations found in m6A regulatory genes are associated with lower OS and EFS rates in patients with AML ( Acute myeloid Leukemia) and presence of p53 mutations.	A:m6A	ALKBH5 FTO METTL14 METTL3 YTHDF1 YTHDF2	Leukemia
METTL3 is overexpressed in AML; Depletion of METTL3 induces cell differentiation and apoptosis and delays leukemia progression; m6A promotes translation of c-MYC, BCL2, PTEN mRNAs in AML. m6A depletion may activate the PI3K/AKT pathway.	A:m6A	METTL3	Leukemia
FTO highly expressed in AML t(11q23)/MLL rearrangements, t(15;17)/PML-RARA, FLT3-ITD and/or NPM1 mutations. FTO enhances leukemic oncogene-mediated cell transformation and leukemogenesis, and inhibits all-trans-retinoic acid (ATRA)-induced AML cell differentiation, through regulating expression of targets such as ASB2 and RARA by reducing m6A levels in these mRNA transcripts.	A:m6A	FTO	Leukemia
YTHDF2 is overexpressed in AML	A:m6A	YTHDF2	Leukemia
FTO promotes AML progression	A:m6A	FTO	Leukemia
YTHDF2 specifically expands human HSC numbers without skewing lineage fate. Essential role of YTHDF2 in regulating HSC self-renewal BY coupling the posttranscriptional m6A modification to the degradation of mRNAs encoding key transcription factors for self renewal (Tal1)	A:m6A	YTHDF2	Leukemia
METTL14 is highly expressed in normal hematopoietic stem/progenitor cells (HSPCs) and acute myeloid leukemia (AML) cells carrying t(11q23), t(15;17), or t(8;21), and is down-regulated during myeloid differentiation. Mechanistically, METTL14 exerts its oncogenic role by regulating its mRNA targets (e.g., MYB and MYC) through m6A modification, which in turn leads to enhanced self-renewal/proliferation of LSCs/LICs and blockage of myeloid differentiation	A:m6A	METTL14	Leukemia
METTl3 is upregulated in H/R-induced cardiomyocytes injury. It methylates TFEB at two m6A residues in the 3ʹ-UTR, and promotes the association of the RNA-binding protein HNRNPD with TFEB pre-mRNA and subsequently decreases the expression levels of TFEB. This inhibits the autophagic flux and increases apoptosis in H/R-treated cardiomyocytes.	A:m6A	METTL3	Ischemic Heart disease
PUS7 mutations result in decreased levels of Ψ13 modifications in tRNAs	U:Y	PUS7	Intellectual disability and progressive microcephaly
A significant reduction in post-transcriptional pseudouridine modification of tRNA in patient cells has occurred.	U:Y	PUS3	Intellectual disability
Loss of function mutation in FTO gene leads to leads to postnatal growth retardation and a significant reduction in adipose tissue and lean body mass	A:m6A	FTO	Intellectual disability
Variants in PUS7 cause the loss of function on pseudouridylation of mRNAs and tRNAs that leads intellectual disabilities.	U:Y	PUS7	Intellectual disability
A mutation on the GRIA2 gene (Q607E) prevents the editing at the Q/R site. Specifically, a cytosine to guanidine base change, immediately 5′ to the adenosine that is edited to inosine by ADAR2, impairs the normal editing of ADARB2. The mutant GAG codon is predicted to be recognized by ADARB2 ~90% less than the normal CAG codon, with a consequent reduction of A:I modifications in the second codon position.	A:I	ADARB2	Intellectual disability
m6A level in circRNAs is decreased in lungs of HPH and in particular, two downregulated m6A circRNAs were identified in HPH: circXpo6 and circTmtc3. Furthermore, m6A level influence the stability of circRNAs, thus affecting circRNA–miRNA–mRNA co-expression network in HPH, resulting in the activation of Wnt and FoxO signaling pathways.	A:m6A		Hypoxia mediated Pulmonary hypertension
m6A level in circRNAs is decreased in lungs of HPH and in particular, two downregulated m6A circRNAs were identified in HPH: circXpo6 and circTmtc3. Furthermore, m6A level influence the stability of circRNAs, thus affecting circRNA–miRNA–mRNA co-expression network in HPH, resulting in the activation of Wnt and FoxO signaling pathways.	A:m6A		Hypoxia mediated Pulmonary hypertension
m6A methylation level decreases the expression of tumor suppressor genes like SOCS2. The upregulation of METTL3 in HCC mediates this event through an m6A-YTHDF2-dependent mechanism and increases cancer cells proliferation, migration and metastasis formation	A:m6A	METTL3	Hepatocellular carcinoma
Two hyper-edited sites (Q103R and K96R) on CDK13 are more abundant in HCC tumor tissues and are associated with poor prognosis in HCC patients	A:I	ADAR	Hepatocellular carcinoma
In mice, overexpression of APOBEC1 determines aberrant editing that could contribute to the oncogenesis	C:U	APOBEC1	Hepatocellular carcinoma
Hyper-editing of FLNB is closely associated with HCC pathogenesis. ADAR1 overexpression increases risk of liver cirrhosis and postoperative recurrence. ADAR1 hyper editing is associated with a poor prognosis	A:I	ADARB1	Hepatocellular carcinoma
Snail, a key transcription factor of EMT, has an increased m6A methylation in its CDS and 3′UTR regions, through METTL3. m6A in CDS of Snail can trigger its translation elongation via interaction with YTHDF1 and eEF-2.	A:m6A	METTL3	Hepatocellular carcinoma
m6A methylation of pri-miR126 enhances its recogntion by DGCR8 and its subsequent processing to mature miRNA. miR126 plays an important role in tumor metastasis by acting as a tumor suppressor. The downregulation of METTL14 in HCC cells leads to the decreased processing of pri-miR126 thus reducing its tumor-suppressor activity	A:m6A	METTL14	Hepatocellular carcinoma
Increased m6A methylation level is associated to a decreased HCC cells proliferation. miR145 targets YTHDF2 3'UTR region and reduces its expression. The reduced expression of YTHDF2 is associated to an increased m6A level in the cells. In HCC cells there is a downregulation of miR145, an increased expression of YTHDF2 which recognize mRNA m6A sites and mediates mRNA degradation (decrease of m6A levels)	A:m6A	YTHDF2	Hepatocellular carcinoma
m6A methylation level decreases the expression of tumor suppressor genes like SOCS2. The upregulation of METTL3 in HCC mediates this event through an m6A-YTHDF2-dependent mechanism and increases cancer cells proliferation, migration and metastasis formation	A:m6A	YTHDF2	Hepatocellular carcinoma
HCC exhibited a characteristic gain of m6A modification in tandem with an increase of mRNA expression, owing to YTHDF2 reduction. YTHDF2 deficiency leads to mRNA stabilization of IL-11 and Serpin E2, the key mediators in support of hypoxia-induced cancer cell survival and vascular reconstruction. YTHDF2 is inhibited by HIF- 2α	A:m6A	YTHDF2	Hepatocellular carcinoma
YTHDF2 was specifically down-regulated by hypoxia in HCC cells, and that YTHDF2 may function as a tumor suppressor in HCC by negatively modulating the EGFR mRNA stability via its binding the m6A site in the EGFR 3’UTR of mRNA, which in turn impairs the MEK/ERK pathway and consequently impedes the cell proliferation and growth	A:m6A	YTHDF2	Hepatocellular carcinoma
YTHDF1 was found to be upregulated in HCC and to play an important role in regulating HCC cell cycle progression and metabolism.	A:m6A	YTHDF1	Hepatocellular carcinoma
Increased m6A methylation (by VIRMA) of ID2 mRNA reduced ID2 expression and promoted cell migration and invasion in HCC	A:m6A	VIRMA	Hepatocellular carcinoma
VIRMA is upregulated in HCC. VIRMA induced m6A methylation on the 3′ UTR of GATA3 pre-mRNA, leading to the separation of the RNA-binding protein HuR and the degradation of GATA3 pre-mRNA, leading to altered GATA3 expression and thereby facilitating the malignant phenotypes of hepatoma cells.	A:m6A	VIRMA	Hepatocellular carcinoma
WTAP is significantly up-regulated in HCC and promotes liver cancer development. WTAP-guided m6A modification contributes to the progression of HCC via the HuR-ETS1-p21/p27 axis. ETS proto-oncogene 1 (ETS1) was identified as the downstream effector of WTAP. The m6A modification regulated by WTAP led to post-transcriptional suppression of ETS1, with the implication of Hu-Antigen R (HuR) as an RNA stabilizer. Then ETS1 was found to inhibit the progression of HCC and could rescue the phenotype induced by WTAP deficiency. Moreover, WTAP modulated the G2/M phase of HCC cells through a p21/p27-dependent pattern mediated by ETS1.	A:m6A	WTAP	Hepatocellular carcinoma
LINC00958 is upregulated in HCC cell lines and tissues. LINC00958 sponges miR-3619-5p which has among its targets HDGF which is important for lipogenesis. LINC00958 is upregulated in HCC cell lines and tissues, thus it icreases the interactions with miR-3619-5p, thus increasing HDGF mRNA expression levels. HDGF has been established as an oncogene that facilitates the progression of HCC. Furthermore, m6A methylation levels are enriched within LINC00958 in HCC cells and they correlate with and increased METTL3 expression level. These results suggest that the increase of LINC00958 in HCC may be attributed to the m6A modification.	A:m6A	METTL3	Hepatocellular carcinoma
Hypo-editing of COPA is closely associated with HCC pathogenesis. ADAR2 downregulation increases the risk of liver cirrhosis and postoperative recurrence. It is associated withpoor prognoses	A:I	ADARB1	Hepatocellular carcinoma
Overexpression of ADAR1 contributes to the alterations in RNA editing patterns, including the editing on FLNB. Moreover, the editing of AZIN1 is responsible for the ADAR1-induced malignant phenotype during ESCC progression	A:I	ADAR	Hepatocellular carcinoma
An increase in RNA editing on AZIN1 neutralizes a key inhibitor of the polyamine synthesis pathway, thereby promoting proliferation in vitro and tumor initiation in vivo. AZIN1 editing is associated with liver cirrhosis	A:I	ADAR	Hepatocellular carcinoma
The m5A distributions in cancer and adjacent tissues showed a noticable difference.	C:m5C		Hepatocellular carcinoma
Hypermethylation of 4506 in 28S subunit of the ribosome leads to ribosome biogenesis deregulation	N:Nm	FBL NOP58	Hemoglobin E
NSUN2 affects the stability and nuclear-cytoplasmic shuttling of mRNAs, non-coding RNAs, and tRNAs.High NSUN2 expression is associated with poor survival rates.	C:m5C	NSUN2	Head and neck squamous cell carcinoma (HNSCC)
Increased m6A methylation protects against GSCs self-renewal, proliferation and tumorigenesis. The increased ALKBH5 expression in GSCs is associated to a decreased methylation of FOXM1 pre-mRNA.	A:m6A	ALKBH5	Glioblastoma
TRM6/61 regulates the translation of a subset of mRNAs encoding proteins that play role in cancer.	A:m1A	Trmt6 Trmt61A	Glioblastoma
Hyperediting at the COG3 I/V site plays a critical pro-tumoral role in GBM and correlates with a worse prognosis in GBM patients	A:I	ADARB1	Glioblastoma
Anti-tumoral: reduction of maturation of oncogenic precursors	C:U	ADARB1	Glioblastoma
Decreased methylation promotes GSCs growth and self-renewal. METTL3 induced methylation protects against GSCs growth and self-renewal	A:m6A	METTL3	Glioblastoma
Decreased methylation promotes GSCs growth and self-renewal. METTL14 induced methylation protects against GSCs growth and self-renewal	A:m6A	METTL14	Glioblastoma
m6A methylation protects against GSCs growth and self-renewal. FTO induced demethylation regulates GSCs growth and self-renewal, promotes tumor progression and shortens the lifespan of GSC-grafted animals.	A:m6A	FTO	Glioblastoma
Increased m6A methylation (mediated by METTL3) induces GSCs mantainance and radioresistence, regulation of alternative splicing events and stability, differential regulation of miRNA and lincRNA, and expression of direct and indirect targets in key glioblastoma-related oncogenic pathways ( NOTCH, NFkB, Wnt, c-Myc, and TGF-b)	A:m6A	METTL3	Glioblastoma
WTAP overexpression increases proliferation, migration, invasion and tumorigenicity of glioblastoma cells	A:m6A	WTAP	Glioblastoma
Reduction of RNA editing at the Q/R site of the GluRB induces loss of Ca2+ homeostasis suggests a role for RNA editing in tumor progression and may provide a molecular model explaining the occurrence of epileptic seizures in association with malignant gliomas.	A:I	ADARB1	Glioblastoma
The overexpression of ADAR inhibits GBM cell line proliferation	A:I	ADAR	Glioblastoma
The overexpression of ADARB1 inhibits GBM cell line proliferation	A:I	ADARB1	Glioblastoma
The reduction of ADARB2 is correlated with the grade of malignancy of glioblastoma multiforme	A:I	ADARB2	Glioblastoma
In tumor samples, dysregulation and genetic alteartions of putative m1A-related enzymes are observed. Also, m1A-related enzymes regulate the ErbB and mTOR pathways.	A:m1A	ALKBH3	Gastrointestinal cancer
ALKBH5 and NEAT1 are upregulated in gastric cancer. The m6A eraser ALKBH5 downregulates NEAT1 m6A levels. With decreases in NEAT1 methylation, NEAT1 is upregulated and promotes the malignant phenotype of GC by acting synergistically with EZH2	A:m6A	ALKBH5	Gastric cancer
Increased m6A methylation level was found to be correlated with the upregulation of METTL3 in GC patients. The increased methylation influences cell proliferation, migration and invasion by regulting transcription factors like GFI-1, apoptotic-related protein expression, AKT signaling pathway (p-AKT, p70S6K and Cyclin D1).	A:m6A	METTL3	Gastric cancer
FTO overexpression in GC tissues was positively correlated with GC histological differentiation, lymph node metastasis and TNM stage. It may promote GC occurrence and its abnormal expression might be associated with GC tumor progression and metastasis. Moreover,in vitro, the viability, proliferation, migration and invasion of GC cells were markedly promoted by the overexpression of FTO	A:m6A	FTO	Gastric cancer
YTHDF2 overexpression in GC cells. Knockdown of YTHDF2 in MGC-803 cells inhibits cell proliferation and promotes apoptosis.	A:m6A	YTHDF2	Gastric cancer
Decreased m6A methylation level, by METTL14 downregulation or FTO upregulation, promotes the activation of oncogenic signaling pathways, such as Wnt and PI3K‐Akt and supports GC cell proliferation, migration and invasion.	A:m6A	METTL14	Gastric cancer
Decreased m6A methylation level, by METTL14 downregulation or FTO upregulation, promotes the activation of oncogenic signaling pathways, such as Wnt and PI3K‐Akt and supports GC cell proliferation, migration and invasion.	A:m6A	FTO	Gastric cancer
NSun2 overexpression is related to poor prognosis.	C:m5C	NSUN2	Gastric cancer
A-to-I RNA editing of the SLC22A3 gene is associated with the reduced SLC22A3 transcription and lymph node metastasis in Esophageal Squamous Cell Carcinoma	A:I	ADARB1	Esophageal squamous cell carcinoma
Increased levels of NSUN2 methylated lncRNA is a key regulator of ESCC tumor metastasis and drug resistance.	C:m5C	NSUN2	Esophageal squamous cell carcinoma
ADARB1 is downregulated in In Esophageal Squamous Cell Carcinoma (ESCC). In normal tissue, ADARB1 suppresses tumor growth and induces apoptosis by editing and stabilizing IGFBP7.	A:I	ADARB1	Esophageal squamous cell carcinoma
~70% of tumor samples from endometrial cancer patients exhibited decreased m6A levels due to either decreased expression of METTL3 or loss of function mutation in METTL14 (R298P). This generates a reduction in m6A mRNA methylation levels and an enhancement in proliferation and tumorigenicity. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator mTORC2. Increased AKT activation is one of the main mediators of increased proliferation in cells.	A:m6A	METTL14	Endometrial cancer
~70% of tumor samples from endometrial cancer patients exhibited decreased m6A levels due to either decreased expression of METTL3 or loss of function mutation in METTL14 (R298P). This generates a reduction in m6A mRNA methylation levels and an enhancement in proliferation and tumorigenicity. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator mTORC2. Increased AKT activation is one of the main mediators of increased proliferation in cells.	A:m6A	METTL3	Endometrial cancer
2′-O-Me-regulated translation is important for cellular growth, differentiation, and hematopoietic stem cell maintenance. Aberrant 2'O-Me is induced by mutations in NPM1 observed in patients with dyskeratosis congenita.	N:Nm	NPM1	Dyskeratosis Congenita
APOBEC1 RNA editing is correlated to a reduction of atherosclerosis thanks to the presence of ApoB48 isoform	C:U	APOBEC1	Diabetes/obesity
RNA editing inhibits the enzymatic activity of TPH2 splice variants. Deregulated alternative splicing and RNA editing are involved in the etiology of psychiatric diseases, such as suicidal behavior.	A:I	ADARB1	Depression disorder
RNA editing inhibits the enzymatic activity of TPH2 splice variants. Deregulated alternative splicing and RNA editing are involved in the etiology of psychiatric diseases, such as suicidal behavior.	C:U	ADARB1	Depression disorder
RNA editing inhibits the enzymatic activity of TPH2 splice variants. Deregulated alternative splicing and RNA editing are involved in the etiology of psychiatric diseases, such as suicidal behavior.	A:I	ADARB1	Depression disorder
RNA editing inhibits the enzymatic activity of TPH2 splice variants. Deregulated alternative splicing and RNA editing are involved in the etiology of psychiatric diseases, such as suicidal behavior.	C:U	ADARB1	Depression disorder
5HT2C editing is altered in suicide victims affected by major depression	A:I		Depression disorder
NSUN3-dependent modification of mt-tRNAMet is a necessary intermediate step towards the formation of 5-formylcytosine (f5C) in mtRNA	C:m5C	NSUN3	Combined mitochondrial respiratory chain complex deficiency
It was found that the negative expression of METTL3 is associated with larger tumor size and higher metastasis rates in CRC. Decreased level of METTL3 increases P38/ERK pathway expression. The increased expression of p-P38 and p-ERK is associated with CRC cells proliferation, migration and invasion.	A:m6A	METTL3	Colorectal cancer
Edited form of RhoQ protein plays an important role in promoting the invasive potential of colorectal cancer	A:I	ADARB1	Colorectal cancer
METTL14 is downregulated in CRC tissues and cell lines. It reduces m6A levels in total RNAs and promotes CRC cell growth and metastasis, METTL14 decreases miR-375 expression levels by modulating DGCR8 binding to primary miR-375 (primiR-375) in a m6A-dependent manner.	A:m6A	METTL14	Colorectal cancer
The increased m6A methylation level in SOX2 transcripts increases SOX2 expression and promotes CRC cells stemness and metastasis. METTL3 is highly expressed in CRC patients, and it induces an increased m6A methylation level in SOX2 transcripts. Methylated SOX2 mRNAs are subsequently recognized by the m6A “reader”, IGF2BP2, which maintains the mRNA stability and expression. Finally, the increased SOX2 expression, through SOX2 downstream targets,npromotes CRC cell stemness and metastasis, leading to CRC progression.	A:m6A	METTL3	Colorectal cancer
The overexpressed YTHDF1, associated to DNA copy number gain, recognizes and promotes the translation of m6A-modified FZD9 and Wnt6 mRNAs, leading to an aberrant activation of Wnt/b-catenin signaling and ultimately affecting the tumorigenicity and stem cell-like activity in CRC. Epigenetic regulation by YTHDF1 plays an important role in cancer progression processes in CRC. In another study, it was demonstrated that YTHDF1 overexpression is promoted by c-Myc and is associated to CRC cells proliferation and chemoresistence.	A:m6A	YTHDF1	Colorectal cancer
The increased m6A methylation level (by METTL3) induces a RP11 accumulation in the nucleus and on chromatin. RP11 increased expression downregulates Siah1 and Fbxo45 and mediates the RP11-induced stabilization of Zeb1 which is fondamental to trigger CRC cells migration, invasion and EMT both in vitro and in vivo.	A:m6A	METTL3	Colorectal cancer
METTL3 is upregulated in colorectal cancer. METTL3 can methylate pri-miR-1246, which further promotes the maturation of pri-miR-1246. The anti-oncogene SPRED2 was identified as the downstream target of miR-1246, wherein downregulated SPRED2 further reverses the inhibition of the MAPK pathway. The METTL3/miR-1246/SPRED2 axis plays an important role in tumor metastasis and provides a new m6A modification pattern in CRC development.	A:m6A	METTL3	Colorectal cancer
YTHDC2 is upregulated in colorectal cancer and it contributes to colon tumor metastasis by promoting translation of HIF-1α	A:m6A	YTHDC2	Colorectal cancer
The m1A distributions in cancer and adjacent tissue showed a noticable difference. Additionally, HGGAGRA and WGGANGA were found as the motifs that have significantly enriched.	A:m1A		Colorectal cancer
A general decrease in editing activity of the human BLCAP transcript in cancerous tissues	A:I	ADAR ADARB1	Colorectal cancer
Upregulation of ADAR1 p-150 isoform, in the blastic crisis of CML, may be related to the activation of inflammatory pathways. An inflammatory mediator-driven isoform switch, which favors ADAR1 p150 expression, drives the expansion of malignant progenitors and contributes to CML progression.	A:I	ADAR	Chronic Myeloid Leukemia
m6A methylation of β-catenin was found to be related to chemo/radiotherapy resistance of CSCC cells. Increased levels of FTO in those cells induce a decreased methylation level in β-catenin and an increased chemo/radiotherapy resistance through the ERCC1 axis.	A:m6A	FTO	Cervical cancer
The two edited forms of BLCAP fail to inhibit STAT3 phosphorylation. A-to-I RNA editing drives anti-tumorigenic BLCAP into a loss-of-function state that might facilitate the events leading to cervical cancer initiation, and progression	A:I	ADAR	Cervical cancer
FTO is frequently overexpressed in human cervical cancer tissues and highly correlated with cervical cancer progression.Mechanistically, FTO directly interacted with E2F1 and Myc mRNAs and inhibition FTO dramatically impaired the translation of these two important oncogenes, thus suppressed cervical cancer cells’ proliferation and migration.	A:m6A	FTO	Cervical cancer
Increased m6A methylation is protecting against cervical cancer cells proliferation and motility. Adenosine methyltransferases are considered as tumorsopressors and adenosine demethylases as oncogenes. Cervical cancer cells were found to have m6A levels significantly reduced.	A:m6A		Cervical cancer
Genetic associations and regulation of expression indicate an independent role for 14q32 snoRNAs in human cardiovascular disease.	N:Nm	FBL	Cardiovascular disease
RNA‐editing of Filamin A pre‐mRNA is decreased in human cardiac disease	A:I	ADARB1	Cardiac Disease
Demethylated tRNA is more sensitive to angiogenin that mediates the cleavage of tRNAs, so tRNA-derived small RNAs are involved in ALKBH3-induced cancer progression by preventing apoptosis of cancer cells.	A:m1A	ALKBH4	Cancer (not specified)
MDAMB468 breast cancer cells were examined to identify m5C epitranscriptome. Differentially methylated sites between breast cancer cells and normal control cell lines were found at CDS and 3`UTRs of mRNA. Genes related to apoptosis and programmed cell death are differentially methylated	C:m5C		Breast cancer
ADAR1 expression is higher in tumor tissues compared to patient-matched normal breast tissues. Silencing of ADAR1 decreases cell proliferation	A:I	ADAR	Breast cancer
Methylation levels on 5.8S, 18S, and 28S rRNAs are slightly increasing in p53 knock-downs.	N:Nm	FBL	Breast cancer
m6A upregulates the levels of HBXIP; increases malignant cell growth and proliferation. METTL3 promoted the expression of HBXIP through m6A modification; high expression of METTL3 is related to increased levels of HBXIP in clinical breast cancer tissues and breast cancer cells; METTL3 increases the levels of expression of HBXIP by affecting m6A modification levels on HBXIP mRNA.METTL3 has increased expression in breast cancer cells and has an essential role in progression.	A:m6A	METTL3	Breast cancer
m6A levels are decreased in immortalized and oncogenically transformed human mammary epithelial cells. The levels of METTL3 are descresed and ALKBH5 are increased. Overexpression of METTL3 and METTL14 and knockdown of ALKBH5 results in increased proliferation and migaration of immortalized cells. m6A levels may be downregulated in immortalized cells. Hypoxia increased m6A levels throgh mechanisms that are independent of METTL3, METTL14 and ALKBH5 expression levels. Increases of m6A levels in hypoxia are regulated by HIF.	A:m6A	ALKBH5 METTL14 METTL3	Breast cancer
m6A modification control the mRNA expression level of NANOG in some breast cancer cell lines. ALKBH5 plays critical role in mediating NANOG expression and BCSC specification and/or maintenance within the hypoxic microenvironment of human breast cancer orthotopic tumors. Mediates (together with Hypoxia-inducible factors (HIFs)) m6A demetylation of NANOG in hypoxic conditions.	A:m6A	ALKBH5	Breast cancer
m6A inhibits breast cancer (BC) cell viability, the ability of MDA-MB-231 cells to form colonies and suppressed cell migratory abilities resulting in an overall effect of inhibition of BC growth and metastasis. Reduced expression of m6A is associated with poor prognostic in patient. Functionally, reducing m6A expression by overexpressing METTL14 and/or knockdown of ALKBH5 could inhibit breast cell viability, colony formation and cell migration.	A:m6A	METTL14	Breast cancer
m6A inhibits breast cancer (BC) cell viability, the ability of MDA-MB-231 cells to form colonies and suppressed cell migratory abilities resulting in an overall effect of inhibition of BC growth and metastasis. Reduced expression of m6A is associated with poor prognostic in patient. Functionally, reducing m6A expression by overexpressing METTL14 and/or knockdown of ALKBH5 could inhibit breast cell viability, colony formation and cell migration.	A:m6A	ALKBH5	Breast cancer
m6A demethylation in the 3' UTR of BNIP3 mRNA leads to its degradation.	A:m6A	FTO	Breast cancer
m6A levels are reduced in breast cancer samples due to a decrease in m6A methylases expression and an increase in demethylases expression; expression levels of METTL3, METTL14, WTAP and FTO were correlated with poor survival and cancer progression; m6A higher levels suppress cancer cell viability, inhibit MDA-MB-231 colony-formation abilities and cell migratory abilities.Expression levels of writers and readers differes according to the subtype of breast cancer ( luminal A/B vs. triple negative).	A:m6A	ALKBH5 FTO METTL14 METTL3 WTAP	Breast cancer
Expression levels of writers, readers and erasers differs between cancer cell lines; no association of the expression levels of METTL3, YTHDF1, WTAP with overall survival was found; HNRNPA2B1 over-expression is associated with poorer overall survival and promotes endocrine resistance;	A:m6A	HNRNPA2B1	Breast cancer
m6A-related targets were altered at protein level; overexpression of the enzymes was associated with poor prognosis on overal survival; YTHDF3 is considered independent prognosis factor for OS and relapse free survival.	A:m6A	VIRMA YTHDF1 YTHDF3	Breast cancer
m6A level are increased in the breast cancer tissue as compared to normal samples; METTL3 overexpression and promotes translation (overexpression) of Bcl-2	A:m6A	METTL3	Breast cancer
Structural brain atrophy in carriers of the FTO risk allele (SNP rs9939609) is identified in healthy elderly subjects . Those carrying at least one copy of the risk allele showed brain tissue deficits in the frontal and the occipital lobes, areas that are also associated with volume reductions in subjects with higher BMI.	A:m6A	FTO	Brain atrophy
WTAP is downregulated in brain AVM lesions compared with normal cerebral vessels. DSP is stabilized via WTAP-m6A-IGF2BPs- dependent manner and participated in the regulation of angiogenesis.	A:m6A	WTAP	Brain arteriovenous malformations (AVMs)
METTL3 is upregulated in bladder cancer cells and tissues. METTL3 could enhance the recognition of pri-miR221/222, which plays an oncogenic role in bladder cancer, by DGCR8 and the subsequent processing to mature miRNAs in an m6A manner.	A:m6A	METTL3	Bladder cancer
METTL3 is upregulated in bladder cancer and m6A level is thus increased. AF4/FMR2 family member 4 (AFF4), two key regulators of NF-κB pathway (IKBKB and RELA) and MYC were further identified as direct targets of METTL3-mediated m6A modification	A:m6A	METTL3	Bladder cancer
METTL3 and CDCP1 are upregulated in bladder cancer patient samples. The increased m6A modification and translation of oncogene CDCP1 in the transformed uroepithelial cells indicates the potential role of METTL3/m6A/CDCP1 axis in bladder cancer oncogenesis.	A:m6A	METTL3	Bladder cancer
m6A modification and METTL14 are lowly expressed in bladder cancer. METTL14 and m6A modification participate in the RNA stability of Notch1 mRNA. Notch1 m6A modification inhibits its RNA stability. Notch1 plays an essential role in bladder tumorigenesis and bladder tumor initiating cells self-renewal	A:m6A	METTL14	Bladder cancer
A general decrease in editing activity of the human BLCAP transcript in cancerous tissues	A:I	ADAR ADARB1	Bladder cancer
hV1.1 recoded by editing (Ile400) is altered in the intracellular side of the selectivity filter	A:I	ADARB1	Behavioral and neurological consequences
Involvement of the FTO SNP rs8050136 in modulating the risk for ADHD	A:m6A	FTO	Attention-deficit/hyperactivity disorder (ADHD)
RNA-editing enzyme ADAR2 occurs in the majority of ALS cases and causes the death of motor neurons	A:I	ADARB1	Amiothrophic Lateral Sclerosis
Defect in the editing of the messenger RNA encoding the GluR2 subunit of glutamate AMPA receptors in ALS patients	A:I	ADARB1	Amiothrophic Lateral Sclerosis
The inefficient GluA2 Q/R site-editing by ADAR2 is one cause of motor neuron death in ALS.	A:I	ADARB1	Amiothrophic Lateral Sclerosis
FTO regulates the phosphorylation of Tau in a mTOR-dependent manner by targeting and reducing the mRNA level of TSC1.	A:m6A	FTO	Alzheimer
Deficiency of RNA editing in Q/R site of the GluA2 induces the loss of Ca2+ homeostasis associated with early onset epilepsy and premature death	A:I	ADARB1	Alzheimer
m6A methyltransferase METTL3 is elevated and the m6A demethylase FTO is decreased in AD mice. The related pathways and genes predicted the potential roles of the differentially expressed m6A methylation RNA in AD.	A:m6A	FTO METTL3	Alzheimer
Alzheimer disease is correlated with a reduction of A to I RNA editing	A:I	ADAR	Alzheimer
2'-O-methylation of the U6 snRNA is impaired; it might influence RNA structure formation and thus splicing fidelity.	N:Nm	LARP7	Alazami syndrome
ADAR1 acts as a suppressor of type I interferon signaling and may have a role in the cytoplasmic accumulation of dsRNA originating from genomic repetitive elements.	A:I	ADARB1	Aicardi-Goutières syndrome
Splicing mutations affecting either the SH2 or PTPase domain of SHP-1 in motheaten and viable motheaten mice lead to multiple hematopoietic abnormalities, including the overexpansion and accumulation of myelomonocytic populations	A:I	ADARB1	Acute Myeloid Leukemia
Decrease in 2'-O-Me due to knock-out of SNORD42A leads to a decrease in ribosomal proteins translation. 2'-O-Me impacts global protein translation by fine-tuning the synthesis of the translational machinery.	N:Nm		Acute Myeloid Leukemia
RNA editing of A3A induces changes in WT1 mRNA which correspond to driver cancer mutations suggests a potential role for this novel modification in cancer mutagenesis	C:U	APOBEC3A	Acute Myeloid Leukemia