In secondary tumors, progression from a low-grade glioma to a GBM involves the serial accumulation of genetic alterations that inactivate tumor suppressor genes such as p53, p16, Rb, and PTEN, or activate oncogenes such as MDM2 and CDKs 4 and 6; alterations in EGFR are less common or absent [8]. This evidence concerns the gene EGFR and glioblastoma.