To date, numerous genetic alterations of oncogene or tumor suppressor genes have been identified in GBM, including EGFR, PDGFRA, PIK3C2B, p16INK4a/p14ARF, PTEN, and RB1 [36], considering that many of these mutations result in an uncontrolled activation of tyrosine kinase receptors (TKR) and their downstream pathways, many efforts have been made to inhibit these deregulated pathways without significant result. This evidence concerns the gene EGFR and glioblastoma.