KMT2A and leukemia: This parallels the origin of therapy-related “secondary” leukemias harboring MLL- rearrangements [4, 6, 7] and is supported by the finding that MLL gene rearrangements can be induced in vitro and in vivo in hematopoietic stem/progenitor cells (HSPCs) at different ontogeny stages by etoposide, a topoisomerase-II inhibitor commonly used in chemotherapy regimens [8–11].