Supplemental 17-β-estradiol (17-βE) interferes with the progression of coronary atherosclerosis and attenuates inflammation in laboratory models of denudative vascular injury and neointima formation [20] as well as in apolipoprotein E-deficient (apo E-/-) mice whose genetically altered lipoprotein metabolism per se predisposes to spontaneous atherosclerotic lesion formation [21]. The gene discussed is APOE; the disease is coronary atherosclerosis.