The phenotype of FH can vary across ancestries as a result of variable penetrance and expression of genetic mutations causing low‐density lipoprotein receptor (LDL‐R) defects; for example, FH could potentially occur as a result of pathogenic somatic mutations in the liver or through vertical transmission due to germinal mosaicism.5, 6. This evidence concerns the gene LDLR and familial hyperaldosteronism.