Analysis of GBM through NGS reveals that the most commonly identified GBM mutations, amplifications, and deletions converge on three key signaling pathways, phosphoinositide-3 kinase/AKT/mammalian target of rapamycin (mTOR), Ras/RAF/mitogen-activated protein kinase, and p53/Rb.4,5,7,32 These include amplifications of genes encoding receptor tyrosine kinases (RTKs), such as PDGFR and EGFR, in proneural and classic-type GBMs, respectively, as well as mutation of TP53, PTEN, and CDK4. Logically, these data spurred drug development efforts focused on these pathways. This evidence concerns the gene EGFR and glioblastoma.