In fact, Lee and coworkers showed that the tumor suppressor gene PTEN (phosphatase and tensin homolog), mutated in 36% of GBMs [30, 31], is able to switch the cell fate of glioma cells exposed to ionizing radiation between apoptosis and senescence, with PTEN-proficient LN18 cells that enter apoptosis, while PTEN-deficient U-87 MG cells, with high levels of both AKT activation and intracellular reactive oxygen species (ROS), undergo senescence after exposure to ionizing radiation [32]. Here, AKT1 is linked to glioma.