Given these considerations and since the discovery of the association between mutations in proprotein convertase subtilisin/kexin type 9 (PCSK9) and familial hypercholesterolemia (FH) in 2003 [12], PCSK9 inhibitors have emerged as the prime candidate to further improve outcomes for CVD patients and may initiate the next revolution in anti-atherosclerotic therapy. Here, PCSK9 is linked to familial hyperaldosteronism.