The molecular pathogenesis of GBM shows recurrent driver somatic mutations in PTEN and p53, epidermal growth factor receptor (EGFR) gene amplification, telomerase reverse transcriptase (TERT) promoter mutation, chromosome 7 gain combined with chromosome 10 loss, and homozygous deletions on CDKN2A/B gene loci, all leading to a dysregulation of core pathways such as the receptor tyrosine kinase (RTK) phosphatidylinositol 3′-kinase (PI3K)/AKT axis, p53, and retinoblastoma (RB) pathways [3,4,5]. The gene discussed is TP53; the disease is glioblastoma.