It is of interest to mention that transgenic mice with high levels of soluble endoglin on any atherosclerotic background (apoE-deficient, LDLR-deficient) are not available and thus we cannot evaluate whether high levels of soluble endoglin might contribute to endothelial dysfunction in atherosclerosis where hypercholesterolemia and inflammation are also present. The gene discussed is LDLR; the disease is familial hypercholesterolemia.