Recent studies have identified a novel small-molecule inhibitor, such as Proprotein convertase subtilisin/kexin type 9, that binds to LDLR in the liver and triggers the degradation of LDLR via the lysosomal pathway and maintains cholesterol homeostasis in the body, to be an innovative pharmacological target for treating hypercholesterolemia and AS [35]. This evidence concerns the gene LDLR and familial hypercholesterolemia.