TP53 and glioblastoma: Another is that the presence of mutations in genes such as epidermal growth factor receptor (EGFR), isocitrate dehydrogenase (IDH), protein kinase C (PKC), tumor protein p53 (p53), phosphatase and tensin homolog (PTEN), retinoblastoma protein (pRB), and vascular endothelial growth factor (VEGF) leads to the deregulation of major cellular pathways, ultimately resulting in high proliferative activity of GBM cells and the promotion of continuous neovascularization in GBM tumors7–10.