Enasidenib, a selective IDH2 inhibitor, also demonstrated promising remission outcomes, driven by differentiation rather than cytotoxicity in patients with IDH2-mutant relapsed or refractory AML (NCT01915498) [65], and proved effective as salvage therapy in heavily treated AML patients (NCT01915498, NCT02577406) [66,67]. The gene discussed is IDH2; the disease is acute myeloid leukemia.