In this sense, patients with familial hypercholesterolemia (FH) caused by pathogenic mutations in the low-density lipoprotein receptor (LDLR) or its associated genes, including apolipoprotein B (APOB), proprotein convertase subtilisin/kexin type 9 (PCSK9), and LDLR adaptor protein 1 (LDLRAP1), are at extremely high risk of CVDs2–4. This evidence concerns the gene LDLR and familial hyperaldosteronism.