The pathophysiology of hypokalemia in Cushing syndrome is thought to be saturation of the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which converts cortisol to inactive cortisone and prevents the cortisol action on the mineralocorticoid receptors [6, 7]. This evidence concerns the gene NR3C2 and Cushing syndrome due to macronodular adrenal hyperplasia.