SETD2 loss drove leukemogenesis when cooperated with NUP93‐HOXD13,[43] while inhibiting MLL‐AF9 AML cell growth both in vitro and in vivo.[44]Ezh2 acts as a tumor suppressor during AML induction, while it exerts an oncogenic function during disease maintenance.[45]. Here, KMT2A is linked to acute myeloid leukemia.