A study that enrolled more than 200 FH patients from the United Kingdom has revealed that the highest numbers of LDLR mutations were located in exons 3 (10%), 4 (28%), 10 (10%), and 14 (21%); 46% of LDLR mutations were detected in the ligand-binding domain (exons 3 to 6), and 46% were detected in the epidermal growth factor precursor-like domain (exons 7 to 14)[6]. This evidence concerns the gene EGF and familial hyperaldosteronism.