Although FH is known to result from deleterious mutations in genes correlated with the LDL receptor pathway, mainly LDL receptor (LDLR), apolipoprotein B (APOB), proprotein convertase subtilisin/kexin type 9 (PCSK9) and low-density lipoprotein receptor adaptor protein 1 (LDLRAP1) [5, 6], genetic testing has seldom been utilized in clinical settings. Here, PCSK9 is linked to familial hyperaldosteronism.