KMT2A and acute myeloid leukemia: Although numerous studies have identified t(11q23)/MLL as a driver mutation that converts HPCs into pre-leukemic stem cells in AML initiation [29–34], the patients with t(11q23)/MLL usually presented with multiple gene alterations at diagnosis, suggesting that other associated mutations might cooperate with t(11q23)/MLL in driving/assisting AML progression [31, 35, 36].