The mechanism of action that leads to FH involves the impairment of the LDL‐R synthesis, defects in transport from endoplasmic reticulum to Golgi bodies, binding with LDL, LDL internalization, recycling of LDL‐R, defect in the apoB‐100 ligand on the LDL and gain‐of‐function mutations causing increased activity of PCSK9.16, 17. Here, PCSK9 is linked to familial hyperaldosteronism.