It has been revealed that defect in LDLR is the most common cause of familial hypercholesterolemia (FH) and premature coronary artery diseases [3], and LDLR-adapter protein 1 (LDLRAP1) and low-density lipoprotein receptor-related protein 6 (LRP6) are required as co-receptors for an efficient endocytosis of LDLR-LDL-C complex in the liver [4, 5]. The gene discussed is LDLR; the disease is familial hyperaldosteronism.