Previous analyses of IDH mutated and 1p/19q codeleted gliomas suggest that protein p16 loss is not a consequence of deletion or mutation of the CDKN2A gene—as found in glioblastomas [24,37]—but rather to epigenetic changes [9,35,36] or impaired protein synthesis [32,33]. This evidence concerns the gene CDKN2A and central nervous system cancer.