CDKN2A and neoplasm: These studies further report the association of GBM with frequent hypermethylation at specific loci, especially at the promoters of several genes involved in GBM pathologies such as MGMT, CDKN2A-p14ARF and CDKN2A-p16INK4a, RB, and TIMP-3, which have direct implications in DNA repair, cell cycle regulation, tumor suppression, and inhibition of apoptosis, respectively (63, 65–67).