In most cases, the pathogenesis of FH is based on a defect in one of three LDL receptor-related genes–APOB, LDLR, and PCSK9. We present our first long-term follow-up RbG study of FH, conducted within the Estonian Biobank (34 recalled participants from a pilot RbG study and 291 controls harboring the same APOB, LDLR, and PCSK9 variants that were included in the pilot study). Here, APOB is linked to familial hyperaldosteronism.