LDLR and familial hyperaldosteronism: Since one of the genetic mutations leading to FH is a loss-of-function mutation in LDL receptors, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are one of the main drugs used to lower LDL cholesterol in patients with FH [6]. HMG-CoA reductase is a rate-limiting enzyme in the synthesis of cholesterol in the liver; therefore, blocking it causes the sensor molecule, sterol regulatory-element binding protein 2 (SREBP2), to increase the expression of LDL receptors on the surface and, as a result, decreases the LDL concentration in the blood [6,7].