Because glucocorticoid can inhibit the Nrf2-dependent antioxidant response and the Nrf2 activator can prevent HF diet-induced obesity and related diseases [15–17], we hypothesize that the activation of Nrf2 could be a therapeutic approach in the prevention of prenatal DEX- and postnatal HF-induced programmed hypertension via the regulation of oxidative stress, SEH, and nutrient sensing. This evidence concerns the gene EPHX2 and hydrops fetalis.