More importantly, immunofluorescence analysis revealed that LXN colocalized with macrophages (labeled by the marker CD68) in aortic lesions (Fig. 1K), indicating that the increase of LXN in atherosclerotic plaques is mainly caused by infiltrating macrophages rather than endothelial cells, which further suggested that macrophages LXN could play an important role in the formation of atherosclerosis. Here, LXN is linked to atherosclerosis.