Increasing evidence has shown that resident macrophages egress poorly from most tissues; therefore, it will be of interest in future studies to address how the egression of VAT macrophages impacts their total numbers and inflammatory potential and whether signals other than netrin‐1 are involved in this egression process.[34] Our previous study showed that CD146 promotes macrophage retention in atherosclerotic plaques and accelerates atherosclerosis development.[19] In this study, we further demonstrate that CD146 promotes the retention of macrophages in the obese state. The gene discussed is MCAM; the disease is atherosclerosis.