Specific driver genetic mutations occur in different subtypes of AML, and therapies targeting mutations in AML have emerged: midostaurin (Stone et al, 2017) in combination with induction chemotherapy for upfront treatment and gilteritinib monotherapy (Perl et al, 2017) for relapsed or refractory disease in AML with FMS‐like tyrosine kinase 3 (FLT3) mutations; and ivosidenib (DiNardo et al, 2018) and enasidenib (Stein et al, 2017) for relapsed or refractory AML with isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) mutations. Here, IDH2 is linked to acute myeloid leukemia.