The selenoprotein glutathione peroxidase 4 (GPX4) is a master regulator of ferroptosis, a form of programmed cell death induced by iron-dependent lipid peroxidation . GPX4 converts lipid hydroperoxides to non-toxic lipid alcohols, therefore preventing ferroptosis . Research studies show that selenium enhances GPX4 expression and inhibits ferroptotic death to protect neurons . In addition, some therapy-resistant cancer cells depend on GPX4 to survive. Loss of GPX4 leads to ferroptosis and thus prevents tumor relapse in mice . Furthermore, redox homeostasis mediated by GPX4 is essential for activation of the cytosolic DNA-sensing cGAS-STING pathway and initiation of the subsequent innate immune response .