In addition, according to the iron hypothesis, excessive iron sequestration within macrophages promotes oxidative reactions and the uptake of lipids due to the down-regulation of ferroportin by hepcidin, and it thus facilitates a macrophage accumulation of plaque, which is demonstrated to lead to vessel wall injury and an increased risk of atherosclerosis [20, 21]. This evidence concerns the gene SLC40A1 and atherosclerosis.