We have previously shown that normal diet-fed SR-B1KO/KOApoEKO/KO mice and HFCC diet-fed SR-B1KO/KOLdlrKO/KO mice (which lack SR-B1 together with either ApoE or Ldlr gene expression) exhibited evidence of platelet accumulation in atherosclerotic coronary arteries, suggesting possible contributions of platelets in driving atherosclerosis development and/or thrombus formation [17,45,50]. This evidence concerns the gene LDLR and atherosclerosis.