The absence of bone marrow compensation, as indicated by the stability of reticulocyte count (Figure 3C), as well as the drop of the mean corpuscular volume (Figure 3D) despite adequate iron store (Figure 3E), were both compatible with the diagnosis of anemia of chronic inflammation, in which increased production of hepcidin, a recently identified acute-phase protein [27], prevents ferroportin from releasing iron stores [28]. The gene discussed is SLC40A1; the disease is anemia.