In addition to solid tumors, for hematological tumors, a series of studies have also reported the regulation of m6A methylation modification in metabolism.For example, the m6A reader IGF2BP2 modulates glutamine metabolism in acute myeloid leukemia (AML), and targeting IGF2BP2 could serve as a novel therapeutic strategy for the disease (108).Moreover, METTL16 drives the development of leukemia and the self-renewal of leukemia stem cells by reprogramming the metabolism of branched-chain amino acids. This evidence concerns the gene METTL16 and acute myeloid leukemia.