This would be consistent with studies in which treatment of ldlr−/− mice with IL-13 resulted in pre-existing plaques the following: an increase in collagen, a reduction in vascular cell adhesion molecule-1 (VCAM-1)-dependent monocyte recruitment, decreased macrophage content, and the induction of M2 macrophages, despite ongoing hyperlipidemia (86). This evidence concerns the gene VCAM1 and hyperlipidemia.