EHMT2 and acute myeloid leukemia: Lehnertz et al. confirmed that G9a facilitated the gene expression of HOXA9-dependent in mouse AML cells through interacting with HOXA9 and recruiting to the sites of HOXA9-dependent genes, and G9a inhibition inhibited AML cell proliferation and induced differentiation [73], suggesting that G9a is a potential target in AML and solid tumors.