The similar vascular phenotypes of these models indicates that the observed alterations are due to the effects of progerin expression, and not to the specific deletion of Apoe or Ldlr. A potential limitation of both the Apoe−/−LmnaG609G/G609G and Ldlr−/−LmnaG609G/G609G mouse models is that the animals develop severe hypercholesterolemia and hypertriglyceridemia, conditions that are generally absent in HGPS patients [13,67], who also show reduced HDL cholesterol levels with age [67]. This evidence concerns the gene LMNA and Hutchinson-Gilford progeria syndrome.