The promyelocytic leukemia–retinoic acid receptor (PML–RAR) fusion, which is seen in approximately 95% of the cases of acute promyelocytic leukemia (APL) (87, 88) can participate in biochemical interactions with several PRC2 complex proteins, recruiting repressive epigenetic modifications on target loci, while the other PML fusion oncoprotein PLZF–RARA binds to PRC1 complex members (89, 90). Here, PRC1 is linked to acute promyelocytic leukemia.