The higher-benefit group comprised slightly over half of the enrolled patients, included those without TP53 mutations, signaling mutations (KRAS/NRAS), or FLT3-ITD, corroborating prior clinical and preclinical findings that these mutations are associated with VEN resistance in AML [55,56,57,58,59,60]. The gene discussed is FLT3; the disease is acute myeloid leukemia.