CDKN2B and neoplasm: These epigenetic alterations converge on silencing critical tumor suppressors, as evidenced by PRMT5 and EZH2 cooperation, which deposits repressive methylation marks such as H4R3me2s, H3R8me2s, and H3K27me3 on the CDKN2B promoter, resulting in transcriptional repression and CpG hypermethylation that favor tumor cell proliferation [69].