On the other hand, coronary artery atherosclerosis and lethal myocardial infarcts develop spontaneously in mice lacking SR-B1 and ApoE (SR-B1/ApoE dKO) [20] and in a high fat/high cholesterol diet-dependent manner in SR-B1/LDLR dKO mice [21] or SR-B1−/− mice with a hypomorphic mutation in apoE [22]. This evidence concerns the gene APOE and coronary atherosclerosis.