More recently, however, genetic inactivation of G9a/GLP in a mouse model as well as pharmacological inhibition in human cells was shown to slow down AML proliferation [26] suggesting that in leukemic stem cells G9a/GLP and H3K9me2 may promote self-renewal and proliferation and that the cellular phenotypes determined by G9A/GLP and H3K9me2 are highly context dependent. The gene discussed is EHMT1; the disease is acute myeloid leukemia.