On the other hand, another study showed that inhibition of DOT1L induces apoptosis of DNMT3A‐mutated AML cells in vitro [57], resulting in diminished expression of key proleukemic genes, including MEIS1. Given all these findings, it is reasonable to speculate that alteration of the Met/SAM pathway and DOT1L inhibition may act synergistically to stop leukemogenesis, particularly in DNMT3A‐mutated and MLL‐rearranged AML. Here, KMT2A is linked to acute myeloid leukemia.