Genetic mutations in 3 FH candidate genes, namely, low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB-100), and proprotein convertase subtilisin/kexin type 9 (PCSK9), are responsible for the autosomal dominant form of FH [2], while other rare mutations in the LDL receptor adaptor protein 1 (LDLRAP1) gene and apolipoprotein E (APOE) gene have been reported to be responsible for the recessive form of FH [3,4]. Here, APOB is linked to familial hyperaldosteronism.