In glioblastoma (GBM), the progression may be associated with alterations in the Wnt, transforming growth factor beta (TGF-β), VEGF, EGFR, cyclin-dependent kinase 2A (CDKN2A), nuclear factor-κB (NF-κB), and phosphatidylinositol-3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathways [47]. Here, AKT1 is linked to glioblastoma.