Despite these similarly broad effects, CDKN2A is often the most functionally relevant target of PRC-mediated repression, as genetic deletion of either the PRC1 component Bmi1 or the PRC2 component Ezh2, or treatment with small molecule inhibitors of EZH2, can facilitate Cdkn2a induction in normal and tumor cells. This evidence concerns the gene PRC1 and neoplasm.