According to studies, inflammation (via cytokines and bacterial lipopolysaccharide, LPS) regulates hepcidin expression and production in response to liver iron levels, hypoxia and anemia, which results in functional iron deficiency or enhanced ferritin and diminished transferrin production, shunting iron to the reticuloendothelial storage pool instead of delivery to erythrocyte precursors [36,37,38]. This evidence concerns the gene HAMP and anemia.