GPX4 and ischemic stroke: The rapid ATP loss during cerebral ischemia leads to uncontrolled ion leakage across cell membranes, causing membrane depolarization and glutamate release.[257, 258, 259] Excessive release of glutamate stimulates its receptors thereby resulting in the activation of phospholipases,[257, 260] phospholipid hydrolysis, AA release,[261] and the loss of repair capacity of GPX4 against lipid peroxide.[262, 263] 12/15‐LOX that directly oxidizes lipid membranes containing PUFAs is a critical regulator of ferroptosis in neuronal damage after ischemic stroke.