A wide variety of genetic alterations that are frequently found in GBM are known to promote the malignant phenotype, including the abnormal activation of the PI3K-AKT and Ras-Raf-MEK-MAPK signaling pathways, the suppression of p53, retinoblastoma protein, and PTEN, as well as the amplification and/or alteration of epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR) [3-5]. This evidence concerns the gene EGFR and glioblastoma.