GPX4 and cancer: Execution converges on three druggable effector hubs—glutathione peroxidase 4 (GPX4) inactivation enabling lipid peroxidation propagation (Yang et al., 2014), System Xc– dysfunction depleting glutathione reserves (Dixon et al., 2012), and p53-mediated iron metabolism reprogramming (Jiang et al., 2015)—that demonstrate epigenetic susceptibility in cancer models, designating them as priority nodes for lncRNA-driven control in neurodegeneration.