Overall, the above findings (see diagram in Figure 4) suggest that endothelial function in the aortas of apoE-/- mice is normal at the early stages of the pathology and the impairment of endothelial NO-mediated dilation occurs at a later stage, mainly in aged animals and when mice are fed an atherogenic Western-type diet, which aggravates hypercholesterolemia and atherosclerosis. The gene discussed is APOE; the disease is familial hypercholesterolemia.