In addition, it was reported by Mehta et al. that ApoE−/− mice lacking hemopexin (Hx) intensified the formation of atherosclerosis via inducing oxidative stress and regulating macrophage function while Hx and ApoE double-knockout (HxE−/−) mice with human Hx injection showed a shift from M1 to M2 macrophages and inhibited the progression of atherosclerosis in ApoE−/− mice [173]. This evidence concerns the gene HPX and atherosclerosis.