It therefore appears that the phenotypic determination of FH based on scores without genotyping for a pathogenic allele on LDLR, APOB, or PCSK9 or without adjusting LDL-C for Lp(a) logically enriches the FH population with patients with hyperlipoprotein(a)emia. The gene discussed is LDLR; the disease is familial hyperaldosteronism.