Several studies have indicated that alterations in m6A modifications contribute to leukemia development: m6A writers (i.e., methyltransferase-like 3 (METTL3) [13, 14], methyltransferase-like 14 (METTL14) [15, 16] and Wilms’ tumor 1-associating protein (WTAP) [17]), erasers (i.e., fat mass and obesity-associated protein (FTO) [18, 19] and α-ketoglutarate-dependent dioxygenase AlkB homolog 5 (ALKBH5) [20, 21]), and readers (i.e., YTH domain family 2 (YTHDF2) [22, 23]) are found to act as oncogenes in AML. The gene discussed is METTL3; the disease is acute myeloid leukemia.