It is caused by mutations with a loss of function in the glucocorticoid receptor (NR3C1), leading to glucocorticoid resistance (increased cortisol, but no clinical signs of hyperfunction) and increased ACTH levels, which leads to the stimulation of adrenal cortical hormone synthesis (aldosterone, cortisol and androgens) and the clinical picture represented by hypertension, hypokalemia, female virilization, premature pubarche, and hirsutism [3]. Here, NR3C1 is linked to Hypokalemia.