In multiple ALI models, the release of inflammatory cytokines contributes to oxidative damage and uncontrolled inflammation and increases intracellular lipid ROS, myeloperoxidase (MPO), and malondialdehyde (MDA) levels which confer resistance to GSH content GPX4 activity, eventually leading to severe mitochondrial damage, presented as obvious ferroptosis [138, 139]. The gene discussed is GPX4; the disease is acute respiratory distress syndrome.