Given the extensive and lethal myocardial infarctions that occur spontaneously at a young age in SR-B1/ApoE dKO mice [20], and in a high fat/high cholesterol diet-dependent manner in SR-B1−/− mice either lacking LDLR or with a hypomorphic mutation in apoE [21,22], we hypothesized that increased susceptibility of cardiomyocytes lacking SR-B1 to cell death may contribute along with the occlusive coronary artery atherosclerosis that develops in these mice to the development of lethal myocardial infarction. This evidence concerns the gene APOE and coronary atherosclerosis.