The molecular progression of gliomas, like many tumors, involves the accumulation of genetic and epigenetic alterations that result in the loss of tumor suppressor gene function (PTEN, TP53, CDKN2A, RB) or the activation of oncogenic pathways (p21–RAS, PI3K, EGFR, CDK4, MDM2) [6–8]. This evidence concerns the gene CDKN2A and central nervous system cancer.