Accordingly, chronic exposures to IL-1β are known to cause anemia through multiple mechanisms38, including attenuation of proliferation and differentiation of erythroid progenitors39, inhibition of erythropoietin production and signaling40, promotion of the biosynthesis of ferritin and down regulation of the expression of ferroportin41, 42, which enable the storage and the release of iron, respectively, by cells such as macrophages and hepatocytes. This evidence concerns the gene IL1B and anemia.