The putative triggers of senescence in our GBM model and in patient GBMs are also known to regulate NRF2 activity such as hypoxia, ROS, PI3K–AKT pathway (enhanced by the loss of PTEN)48,59 or Nrf2 transcription such as RAS oncogene (K-RAS)60. This evidence concerns the gene PTEN and glioblastoma.