Although they are widely used, these models do not capture the full biology of the corresponding human Mendelian diseases, familial dysbetalipoproteinemia (in the case of Apoe), and familial hypercholesterolemia (in the case of Ldlr): the HDL-cholesterol in both Apoe−/− or Ldlr−/− mice is still higher than in humans with APOE2/2 or LDLR−/− genotypes, and in both models, it is mainly the VLDL (and not the IDL and LDL, respectively) that increases. Here, APOE is linked to familial hypercholesterolemia.