The findings indicated that after knocking down PGC‐1α, the proliferation of K562 cells decreased, apoptosis increased, and differentiation into monocytes and myeloid lines increased (Figure 6A–F), suggesting that PGC‐1α may act as an oncogene in AML and that these phenotypes are similar to the effects of METTL3 knockdown on AML cells [22, 59]. This evidence concerns the gene METTL3 and acute myeloid leukemia.