Increased abundance of m6A by METTL3 enhances cell growth and represses myeloid differentiation in acute myeloid leukemia (AML).[29, 30] Meanwhile, FTO is involved in delayed differentiation and induces cellular apoptosis in AML.[31] The essentiality and reversibility of m6A regulators make them promising therapeutic targets for small molecule inhibitors. Here, METTL3 is linked to acute myeloid leukemia.