In GBM, homozygous deletions of CDKN2A (ARF/56%), gene amplification of MDM2/4 (8.2%/9.4%) and missense mutations in TP53 (31.5%) all lead to loss of p53 tumor suppressive functions, either through reduced activity or through reduced levels (TCGA, PanCancer Atlas). This evidence concerns the gene TP53 and glioblastoma.