There are several gene mutations of the LDLR that lead to mild or severity FH, such as mutations that affect the synthesis of the LDLR in the endoplasmic reticulum, mutations that disable proper transport of LDLR to the Golgi apparatus, mutations that disable binding of LDL-C to the LDLR, mutations that disable the receptor-ligand complex internationalization, and mutations that disable proper recycling of LDLR [31,32,33]. This evidence concerns the gene LDLR and familial hyperaldosteronism.