As shown in Fig. 5a–c, treatment of AML cells with 2–8 mM dimethyl-αKG (DM-αKG, a cell-permeable derivative of α-KG) strongly induced apoptosis, suggesting that elevated intracellular α-KG per se was sufficient to have a major impact on AML cell survival, and the cytotoxic effect of IDH2 knockdown could be attributed, at least in part, to the abnormal accumulation of α-KG. The gene discussed is IDH2; the disease is acute myeloid leukemia.