By contrast, dual inhibition of EZH2 and G9A/GLP histone methyltransferases by substrate-competitive HKMTI-1-005 promotes myeloid differentiation of AML cells, potentially by selectively interfering with the canonical PRC2-related activities of EZH2 while permitting non-canonical, pro-differentiative activity. This evidence concerns the gene EZH2 and acute myeloid leukemia.