KMT2A and acute myeloid leukemia: It suggests that LSD1 might regulate myeloid differentiation and oncogenic proliferation on at least three dimensions: the first one is histone modification, such as H3K4 methylation; the second is non-histone protein methylation, such as p53-K372 methylation; and the last one is non-enzymatic scaffolding function, such as LSD1-GFI1 interaction in MLL-AF9 translocated AML, indicating the complexity of LSD1 function in the different cell contexts.