The cKO of Gpx4, which is expressed at higher levels in the proximal tubular cells than it is in the glomeruli, caused AKI with increased phosphatidylcholine (PC)-, phsphatidylethanolamine (PE)-, and cardiolipin (CL)-esterified linoleic acid (LA, C18:2), arachidonic acid (AA, C20:4), and docosahexaenoic acid (DHA, C22:6) oxidations, while Gpx4 KO mice showed embryonic lethality [105,110]. This evidence concerns the gene GPX4 and acute kidney injury.