Hypertension in Cushing’s syndrome arises from complex mechanisms, including the activation of mineralocorticoid receptors when cortisol levels exceed the capacity of 11β-hydroxysteroid dehydrogenase type 2 to inactivate cortisol into cortisone, leading to sodium retention, potassium excretion and blood volume expansion, resulting in apparent mineralocorticoid excess and suppressed renin secretion. The gene discussed is REN; the disease is Increased circulating aldosterone concentration.