AKT1 and glioblastoma: This involves the overactivation of the RAS/RAF, mitogen-activated protein kinase (MEK), extracellular-signal-regulated kinase (ERK), and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathways, by activating tyrosine kinase receptors such as the epidermal growth factor receptor (EGFR), the platelet-derived growth factor receptor (PDGR), and the vascular endothelial growth factor receptor (VEGFR), which have been found upregulated in GBM [7,8,9].