Serum Lp(a) levels in familial hypercholesterolemia with LDLR mutations have been shown to be elevated, suggesting that Lp(a) is catabolized via the LDLR pathway [28]; however, statins, whose main mechanism of action involves the upregulation of LDLR, are unable to reduce Lp(a) levels effectively [29]. This evidence concerns the gene LDLR and familial hypercholesterolemia.