The mechanism by which increased BCAT1 expression drives the progression of the glioblastoma subtype represented by A11 has been shown here to be similar to that observed in AML stem cells.5 Knockdown of BCAT1 resulted in the accumulation of α-KG, leading to the degradation of HIF-1α, whereas overexpression of BCAT1 decreased α-KG concentrations, stabilizing HIF-1α and resulting in DNA hypermethylation through decreased TET activity. Here, BCAT1 is linked to acute myeloid leukemia.