Our recent studies indicate that early postnatal treatment targeting the arachidonic acid metabolism pathway by using a soluble epoxide hydrolase (SEH) inhibitor 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA) ameliorates programmed hypertension in both programming models of maternal high-fructose consumption and prenatal dexamethasone exposure [113,114]. Here, EPHX2 is linked to hypertensive disorder.