AKT1 and glioblastoma: Interestingly, EGFR-MAPK and PI3K-AKT-mTOR signaling is hyperactivated in glioblastoma by EGFR amplification, mutation of the MAPK pathway inhibitor Neurofibromin 1 and loss of the phosphatase and tensin homolog (PTEN) [5,11,53] and is associated with resistance to radiation therapy in glioblastoma [14].