The genetic lesions inherent in glioblastoma have been shown to affect telomere length, chromatin regulation, and intracellular signaling, involving receptor tyrosine kinases (epidermal growth factor receptor (EGFR), FGFR, BRAF), mitogen-activated protein kinase, and phosphoinositide-3-kinase (PI3K/AKT/mTOR), as well as the retinoblastoma/E2F and the p53 tumor suppressor pathways [23,24,25]. The gene discussed is AKT1; the disease is glioblastoma.