Since G9a/GLP, the histone methyltransferase specific for H3K9me2, is involved in repression of several genes associated with AML [24, 25] and contributes to AML progression [26], we asked if we could reverse formation of AML-specific H3K9me2 blocks in human myeloid cells using a pharmacological G9a inhibitor UNC0638 [67]. This evidence concerns the gene PRDM9 and acute myeloid leukemia.