Bai et al. have generated macrophage-specific MED1/apolipoprotein E (ApoE) double-deficient (MED1ΔMac/ApoE−/−) mice and found that MED1 ablation decreased the binding of peroxisome proliferator-activated receptor γ (PPARγ), which promoted the polarization of macrophages from M2 to M1 and enhanced innate immune stimulation, thereby increasing atherosclerosis [57]. This evidence concerns the gene MED1 and atherosclerosis.