Probucol is efficient in LDLR-deficient animal models and familial hypercholesterolemia (FH) patients as well as in reducing the synthesis of apoB, which is a major structural protein of LDL essential for recognizing LDLR that reduces nascent particle formation and promotes LDL clearance (Frikke-Schmidt et al., 2008). Here, LDLR is linked to familial hyperaldosteronism.