Previously, GR haploinsufficient rats that developed salt-sensitive hypertension exhibited dysregulation of adrenal sEH, leading to a plasmatic elevation of several less active diol metabolites (DiHETrEs) highly suggested an association of sEH with primary generalized glucocorticoid resistance in rats with hypercortisolism and mineralocorticoid access [52]. This evidence concerns the gene EPHX2 and adrenal gland hyperfunction.