Prominent genomic alterations frequently found in GBM include loss-of-function of tumor suppressors in the p53, phosphatase and tensin homolog and neurofibromatosis 1, and hyperactivation of receptor tyrosine kinase (RTK) signaling, including EGFR, PDGF receptor, and the receptor for hepatocyte growth factor (Met) [3]. Here, PTEN is linked to glioblastoma.