An analysis of samples from a phase I trial in patients with relapsed/refractory AML and either IDH2R140 or IDH2R172 confirmed enasidenib’s potent suppression of 2-HG and normalization of hematopoietic differentiation, including emergence of functional IDH2-mutated neutrophils [89]. The gene discussed is IDH2; the disease is acute myeloid leukemia.