TP53 and acute myeloid leukemia: Potential reasons include frequent clonal hematopoiesis and depletion of hematopoietic reserve leading to slower hematologic recovery following intensive remission-induction chemotherapy, the possibility of primary disease recurrence in case of s-AML occurring after a prior malignant disease or MDS and higher incidence of poor-risk cytogenetics and of TP53 mutations in s-AML than in de novo AML patients [4,5,6].