It is speculated that the classical p62-mediated NRF2 activation pathway plays the major regulatory role in p53-WT GBM, thus resulting in the suppression of ferroptosis; while p62-mediated p53-SLC7A11 axis plays the major regulatory role in p53-mutant GBM, consistent with stronger mutant-p53-NRF2 association mediated by p62 and enhanced inhibition of NRF2 antioxidant activity, leading to the induction of ferroptosis. This evidence concerns the gene SLC7A11 and glioblastoma.