Considering that angiotensin II (Ang II) accelerates the development of atherosclerosis in both LDL receptor-/- and apoE-/- mice [33,49,50] and that hypercholesterolemia has been associated with activation of the renin-angiotensin system [51,52], the apoE-/- mouse became an exciting model for evaluating the hemodynamic effects of Ang II in hypercholesterolemic mice (see a hypothetical mechanism in Figure 1). This evidence concerns the gene AGT and familial hypercholesterolemia.