AKT1 and glioblastoma: On a molecular level, glioblastoma exhibits frequent overactivation of growth factors—such as epidermal growth factor receptor (EGFR), platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF)—and associated signaling pathways, including phosphatidylinositol 3-kinases (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), and mitogen-activated protein kinase (MAPK).