While accelerated injury- and transplant-based atherosclerosis, as well as spontaneous genetic models of Type II familial hypercholesterolemia (FH), the most frequent type of FH observed in humans that leads to atherosclerosis, are continually emerging, the most widely studied murine models of FH-mediated human atherosclerosis are the low density lipoprotein receptor-deficient (Ldlr−/−) [3] and apoE deficient (Apoe−/−) [4–6] mouse lines. The gene discussed is VLDLR; the disease is familial hyperaldosteronism.