The TCGA studies also revealed that the molecular abnormalities in GBM preferentially align in certain pathways including the activation of the epidermal growth factor receptor (EGFR) along with other tyrosin kinase receptors-initiated signaling pathways, the tumor protein 53 (TP53) and retinoblastoma (RB1) pathways [13–17]. This evidence concerns the gene TP53 and glioblastoma.