Since oxidative stress plays a crucial role in the pathogenesis of atherosclerosis [22], we examined whether macrophage-specific Fpn1 deficiency-mediated iron retention increased ROS levels in the aortas of Apoe−/−Fpn1LysM/LysM mice by performing dihydroethidium (DHE) fluorescence staining and measuring malondialdehyde (MDA) content. This evidence concerns the gene SLC40A1 and atherosclerosis.