The most accurate prognostic stratification is based on cytogenetics, further refined with the analysis of several gene mutations.1, 2, 3, 4 In cytogenetic intermediate-risk AML (IR-AML), comprising ~50% of all AML patients, the mutational status of NPM1, internal tandem duplication of FLT3 (FLT3-ITD), and CEBPA defines molecular subcategories with different biological risk and diverse outcomes.2, 4 Therefore, many current AML treatment protocols adapt their therapeutic algorithm to this biological risk. The gene discussed is NPM1; the disease is acute myeloid leukemia.