Conversely, in obesity and atherosclerosis, expression of netrin-1 and its receptor Unc5b are upregulated in tissue macrophages in response to lipid and oxidative stressors, and can prevent resolution of inflammation by inhibiting macrophage responses to chemokines (e.g., CCL19, CCL21) directing the egress of inflammatory macrophages from tissues and preventing macrophage apoptosis [37–39]. This evidence concerns the gene NTN1 and atherosclerosis.