The vast majority of primary GBM is driven by a genetic mutation in key tumor suppressor genes concomitant with the accelerated activity of different proto-oncogenic signaling pathways (e.g., epidermal growth factor receptor, EGFR, or platelet- derived growth factor receptor-A, PDGFRA) or through a mutant (ligand-independent) form of EGFR (EGFR-variant-3, EGFRvIII) [1]. This evidence concerns the gene EGFR and glioblastoma.