In fact, multiple points within the p53 signaling pathways are disrupted in GBM due to missense mutations and/or amplification, the overexpression of MDM2, and/or loss of expression of the p16Ink4-p14ARF locus, all of which block p53 activity and lead to uncontrolled glial cell proliferation and brain oncogenesis. This evidence concerns the gene CDKN2A and glioblastoma.