Furthermore, overexpression of CHAF1B in MLL::AF9 fusion oncoprotein-expressing cells drastically enhanced leukemia development in mice, while the deletion of this chaperone subunit induced differentiation of MLL::AF9 AML cells.67 These results highlight the CAF-1 canonical histone chaperone acting as an important molecular switch, regulating normal hematopoiesis and leukemogenesis. Here, CHAF1B is linked to acute myeloid leukemia.