In mouse models of CKD, knockout of sEH increased EET bioavailability and prevented inflammation and renal tubulointerstitial fibrosis by activating PPAR isoforms and downregulating TGF-β1/Smad3, NF-κB, and inflammatory signaling pathways (Imig et al., 1996; Kim et al., 2014). Here, EPHX2 is linked to chronic kidney disease.