While the details differ—AML sees BCAT1 limiting α-KG (resulting in hypermethylation), whereas NSCLC sees BCAT1 increasing α-KG (resulting in hypomethylation)—both cases illustrate that dysregulated BCAA metabolism can lock cells into a malignant state via epigenetic mechanisms. The gene discussed is BCAT1; the disease is acute myeloid leukemia.