In AML stem cells BCAT1 upregulation lowers α-KG concentration, resulting in reduced activity of α-KG-dependent dioxygenases, including Ten Eleven Translocation (TET) enzymes and Egl-9 Hypoxia Inducible Factor 1 (Egln1), leading to a hypermethylated DNA state, similar to that in IDH mutant cells, and stabilization of HIF-1α, respectively.5 Treatment of A11 cells with dimethyl α-KG, a cell-permeable analog of α-KG,34–36 mimicked the effects of BCAT1 knockdown on cell proliferation (Figure 5G). The gene discussed is EGLN1; the disease is acute myeloid leukemia.