In myeloid precursors, the PAX5 gene is normally repressed by a polycomb-repressive complex; however, in AML with RUNX1::RUNX1T1, aberrant mitogen-activated protein kinase (MAPK) signaling, enabled by mutations of KIT, RAS or FLT3, lead to the dissociation of the polycomb repressive complex from the PAX5 promoter, supporting its expression [10]. This evidence concerns the gene FLT3 and acute myeloid leukemia.