Major causes of FH are loss-of-function mutations in the low-density lipoprotein (LDL) receptor (LDL-R) or apolipoprotein B-100 (apo B) gene, or gain-of-function mutations in proprotein convertase subtilisin/kexin type 9 (PCSK9), resulting in very high blood cholesterol levels and premature CVD [1,2]. Here, APOB is linked to familial hyperaldosteronism.