Recently, Vinchi et al. showed that, in the presence of genetic iron overload caused by a heterozygous mutation of iron exporter Ferroportin C326S, Apoe−/− mice develop severe spontaneous atherosclerosis in the absence of a high-fat diet, which can be rescued by iron restriction (low-iron diet or iron chelator deferasirox) [477]. The gene discussed is APOE; the disease is atherosclerosis.