The enzyme hydroxysteroid dehydrogenase type-I (HDS1) converts cortisone to cortisol within insulin target tissue, such as liver, visceral adipose tissue and skeletal muscle, resulting in local GC action which by promoting adipogenesis [26] leads to IR and subsequently hyperinsulinemia; this in turn along with other adipokines results in increased aldosterone production, Na+ retention, and HTN [27]. The gene discussed is INS; the disease is Hyperinsulinemia.