TP53 and glioblastoma: 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.