Apolipoprotein B (APOB) helps the LDLR bind LDL, while proprotein convertase subtilisin/kexin type 9 (PCSK9) degrades the LDLR; mutations in the respective APOB and PCSK9 genes account for 5 and <1% of FH cases, respectively. This evidence concerns the gene APOB and familial hyperaldosteronism.