The m6A writers [methyltransferase-like 3 (METTL3), methyltransferase-like 14 (METTL14)], erasers [α-ketoglutarate-dependent dioxygenase AlkB homolog 5 (ALKBH5), and fat mass and obesity-associated protein (FTO)], highly expressed in AML, were involved in the development, differentiation, progression, and maintenance of AML through various m6A-dependent mechanisms (Barbieri et al., 2017; Li et al., 2017; Vu et al., 2017; Weng et al., 2018; Shen et al., 2020). This evidence concerns the gene METTL3 and acute myeloid leukemia.