LDLR and familial hyperaldosteronism: FH primarily arises from genetic mutations leading to the impaired function of the gene that encodes the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB) genes, or the increased function of the proprotein convertase subtilisin/kexin type 9 (PCSK9) gene [22,23,24,25,26].