More than 90% of the patients with genetically confirmed FH have mutations in the gene encoding the LDL-C receptor (LDLR), and a lower percentage of FH diagnoses are associated with alterations in genes encoding apolipoprotein B (ApoB), proprotein convertase subtilisin–kexin type 9 (PCSK9), or LDL receptor adaptor protein 1 (LDLRAP1) [9]. Here, LDLR is linked to familial hyperaldosteronism.