KMT2A and acute myeloid leukemia: In the pathogenesis of t-AML, distinct mechanisms were reported, such as direct induction of a fusion oncogene such as PML/RARA or MLL gene mediated by TI [28, 29], selective expansion of preexisting clonal hematopoiesis with TP53 mutation [30–32], and chemotherapy-induced alterations to the bone marrow microenvironment [33].