The FH is mainly due to the presence of loss‐of‐function variants in low density lipoprotein receptor (LDLR) gene (MIM: 606945), while loss‐of‐function variants in apolipoprotein B (APOB) gene (MIM: 107730) and gain‐of‐function variants in proprotein convertase subtilisin/kexin type 9 (PCSK9) gene (MIM: 607786) are less frequently.4 This evidence concerns the gene PCSK9 and familial hyperaldosteronism.