SLC7A11 and glioblastoma: In p53-mutant GBM, the stronger interaction of mutant p53/NRF2 with p62 enhanced the inhibitory effect of mutant p53 on NRF2 signaling and reversed the classical p62-mediated NRF2 activation pathway, while p62 increased the transcriptional inhibition of SLC7A11 by p53, leading to the reduction of SLC7A11 and acting as a proapoptotic inducer.