A model of the pathophysiology of the anemia of inflammation based on the findings in Kim et al and Gardenghi et al.^1,2 Injection of heat-killed B abortus stimulates an inflammatory response including increased production of hepcidin and IL-6. Hepcidin binds to the iron exporter ferroportin resulting in internalization of the protein, increased macrophage iron storage, and subsequent hypoferremia. Recovery from the inflammatory response lowers hepcidin and IL-6 levels leading to increased release of iron from the macrophages to the developing erythrocytes and relief of the block in erythroid development. Fpn, ferroportin.