SAP30 hijacked the methyltransferase MLL1 to the SIN3 protein complex, which increased trimethyl lysine 4 of histone H3 (H3K4me3), chromatin accessibility, and RNA polymerase II occupancy at the promoters, thereby switching on cancer gene expression and promoting breast tumor development in the mouse models. The gene discussed is KMT2A; the disease is breast neoplasm.