METTL16 incorporates m6A modification into branched‐chain amino acid transaminases (BCAT1 and BCAT2), upregulating their expression thereby causing metabolic reprogramming of AML cells as well as maintaining LSC/LIC self‐renewal.[43] The m6A‐binding protein, IGF2BP2, an m6A reader, promotes the self‐renewal capability of LSCs/LICs by modulating the metabolic programming of the cells. Here, METTL3 is linked to acute myeloid leukemia.