Although the co-existent aberrations, such as nucleophosmin 1 (NPM1) mutation and internal tandem duplication of fms-like tyrosine kinase 3 (FLT3-ITD), have a clear impact on clinical aggressiveness of IDH1/2-mutated (IDH1/2+) leukemias, even in a selected NPM1/FLT3-ITD NK-AML subpopulation, the prognostic impact of IDH1/2 mutations is still very heterogenous, and the factors responsible for such prognostic discrepancies are not fully understood2,6–10. The gene discussed is FLT3; the disease is leukemia.