According to several studies on humans, FH is an autosomal dominant hereditary disorder with a gene prescription impact and is triggered by mutations in the intended genes encoding the PCSK9, apolipoprotein B (APOB), or LDL receptor (LDLR), with mutations in each such gene accounting for 1, 5, and 90% of FH cases, respectively (Hobbs et al., 1992; Defesche et al., 2017; Zhao et al., 2020). This evidence concerns the gene APOB and familial hyperaldosteronism.