Our results indicate that hypoxia maintains mTOR pathway in an inactive state and this occurs by preserving HIF-1α stability, whereas an acute exposure to high oxygen tension and/or BMP2 treatment promote activation of Akt/mTOR and down stream dependent pro-translational and pro-differentiating responses in GBM cells, which undergo a metabolic shift, as shown by increased of succinate dehydrogenase (SDH) activity following these stimuli. Here, AKT1 is linked to glioblastoma.