Particular mention should be made of the promotion of differentiation of leukemic blasts in a sizeable subset of R/R FLT3 patients [62], which has also been reported in patients treated with IDH-mutant AML treated with IDH inhibitors (enasidenib and ivosidenib), for the induction of QT prolongation, pancreatitis, embryo–fetal toxicity, and a rare neurologic complication: posterior reversible encephalopathy syndrome (PRES), which requires permanent discontinuation of the drug. The gene discussed is FLT3; the disease is acute myeloid leukemia.