In therapy-related myeloid malignancies, TP53 mutations are not induced by the treatment itself but by existing progenitor clones with mutant TP53, that are resistant to DNA-damaging therapy, and expand in clonal hematopoiesis to give raise to TP53-mutated MDS/AML (Fig. 1b) [1]. The gene discussed is TP53; the disease is myelodysplastic syndrome.