It is well established that PPARγ activates reverse cholesterol transport in lesion‐resident macrophages.37–38 Furthermore, PPARγ ligands promote the reduction of atherosclerotic lesions,50–51 whereas the conditional knockout of macrophage PPARγ enhances atherosclerosis without altering plasma lipid levels.52 We observed increased cholesterol efflux as well as increased expression of ABCG1 in TDAG51−/− peritoneal macrophages. Here, PPARG is linked to atherosclerosis.