Enasidenib, an inhibitor of mutated IDH2, restored normal enzyme activity and induced differentiation and durable remissions even in elderly patients with multiple comorbidities4–6, ivosidenib, an inhibitor of mutated IDH1, induced myeloid differentiation of AML blasts and durable remissions in patients with newly diagnosed IDH1-mutant AML ineligible for standard chemotherapy7, and gilteritinib, a type I FLT3 inhibitor, induced differentiation in relapsed and refractory FLT3-mutated AML8. The gene discussed is IDH1; the disease is acute myeloid leukemia.