For example, in mineralocorticoid-responsive tissues such as the kidney and colon, MR are protected from exposure to the high-affinity ligand cortisol by 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2)9, which converts cortisol to inert cortisone; inhibition of 11β-HSD2 results in cortisol-dependent excessive MR activation and hypertension. This evidence concerns the gene NR3C2 and Hypertension.