Autosomal dominant variants in the LDL receptor gene (LDLR) represent the most common cause of FH and for decades were recognized as a single etiology of monogenic FH.1 Later, identification of causative variants in the apolipoprotein B gene (APOB), and more recently in the proprotein convertase subtilisin kexin 9 gene (PCSK9), expanded the list of FH causal genes. Here, LDLR is linked to familial hyperaldosteronism.