AKT1 and glioblastoma: Moreover, the EGFR downstream pathways phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-AKT-mechanistic target of rapamycin kinase (mTOR) signaling and mitogen-activated protein kinase (MAPK) signaling are prominently deregulated and favor therapy resistance in glioblastoma [14,15].