However, it has been revealed that proprotein convertase subtilisin kexin type 9 (PCSK9) could mediate LDLR degradation by binding to the epidermal growth factor (A) and β-propeller domains of LDLR [7,8,9], thereby, PCSK9 has been now recognized as an attractive therapeutic target for hypercholesterolemia. This evidence concerns the gene PCSK9 and Hypercholesterolemia.