To date, pathogenic variants causing FH are predominantly reported in three genes: low-density lipoprotein receptor (LDLR), 95%; apolipoprotein B (APOB), 2–11%; and proprotein convertase subtilisin/kexin type 9 (PCSK9), 1% [1, 8, 9, 12]. The gene discussed is LDLR; the disease is familial hyperaldosteronism.