However, as more genotyping of FH patients was carried, patients with the phenotype but no LDLR mutation were discovered, and the search for other genes yielded the discovery of the Apolipoprotein B gene (ApoB) in 1987 [5], and the Proprotein Convertase Subtilin/Kexin 9 gene (PCSK9) in 2003 [6], as candidate genes in ADH. This evidence concerns the gene LDLR and familial hyperaldosteronism.