In both mouse atherosclerosis models [e.g., animals deficient for apolipoprotein E (ApoE) or LDL receptor (Ldlr)], treatment with IFN-I enhanced atherogenesis associated with increase in lesion numbers and plaque size, macrophage-endothelial cell adhesion, and leukocyte attraction to inflamed vascular sites (Levy et al., 2003; Goossens et al., 2010). This evidence concerns the gene LDLR and atherosclerosis.