LDLR and familial hyperaldosteronism: Several studies showed that LDLR null mutations protected pancreatic β-cells from cholesterol accumulation and thus a reduced risk of insulin resistance have been observed in these subjects [6, 7]; however, defective LDLR mutations or mutations in other FH genes could contribute to a cholesterol-induced metabolic dysfunction in FH subjects with a residual/normal LDLR activity [8].