This result agrees with the mice report which described that G2A deletion on Apoe–/– or Ldlr–/– background contributed to aortic macrophage accumulation and increased atherosclerotic plaques (Bolick et al., 2009), but it is in contrast to the other two in Ldlr–/– model which found that mice G2A deficiency attenuated atherosclerosis (Parks et al., 2006, 2009). This evidence concerns the gene APOE and atherosclerosis.