In line with this, we demonstrated that GPX7 was overexpressed in glioma cell lines in a cell cycle-dependent manner and was higher in patients harboring mutations in TP53 and EGFR, suggesting its involvement in cancer cell growth associated with a response to a progressive accumulation of ROS, probably driven by mutant TP53 and EGFR combined with a metabolic reconfiguration and a coordinated regulation of other factors present in the glioma TME (e.g. hypoxia, inflammatory cytokines, growth factors)109,119. Here, GPX7 is linked to glioma.