This is observed especially in the era of newer and targeted therapies, like liposomal daunorubicin and cytarabine (Vyxeos) for high-risk/secondary AML [18], venetoclax combined with hypomethylating agents [2,19,20,21,22], gemtuzumab ozogamicin (GO) for favorable risk AML [23], FLT3 inhibitors with or without chemotherapy for AML with FLT3 mutation [24,25,26], ivosidenib and azacitidine in IDH1-mutated acute myeloid leukemia [8,27], IDH2 inhibition in IDH-mutated AML [28], and menin inhibitors targeting driver mutations in AML such as KMT2A and NPM1 [29,30,31,32]. The gene discussed is IDH2; the disease is acute myeloid leukemia.