LDLR and familial hyperaldosteronism: In rare (less than 0.5%) of FH patients, a missense gain-of-function mutation in the PCSK9 gene results in elevated plasma PCSK9 levels, increased LDLR degradation and impaired recycling leading to reduced LDLR-mediated clearance of LDL-C from the bloodstream and increased plasma LDL-C levels [76, 77].