AKT1 and glioblastoma: In comparison, Ludwig et al. recently demonstrated that hypoxic and radiation induced the activity of NOX along with ROS generation, resulting in inactivation of phosphate and tensin homolog (PTEN) and enhancement of Akt phosphorylation, and ultimately promoted survival of PTEN-expressing GBM cells in vitro and in vivo, suggesting that inhibition of NOX activation is a potential therapeutic target in PTEN-functional GBM [74].