In the present study, we found that ApoE deficiency has no significant effect on the expression of hepcidin (and also Fpn1) in ApoE–/– mice, being consistent with what was reported by Kautz et al. (67), namely hepcidin expression was not increased at any stage of atherosclerosis progression in ApoE–/– mice. The gene discussed is SLC40A1; the disease is atherosclerosis.