Patients with cushing syndrome have 11-b hydroxysteroid dehydrogenase deficiency, which reduces the amount of cortisol involved in metabolism and conversion into cortisone, and increases the amount of combined with mineralocorticoid receptor, thus enhancing the effect of mineralocorticoid like on the epithelial cells of distal convoluted tubules and collecting ducts, causing increased potassium excretion and sodium retention, leading to hypokalemia and hypertension.[12] The merger of GS with non ACTH dependent CS and adrenal cortisol secreting adenoma has not been reported in the past. The gene discussed is NR3C2; the disease is Cushing syndrome due to macronodular adrenal hyperplasia.