Hepcidin (Hepc, hepatic bactericidal protein) or LEAP (liver expressed antimicrobial peptide) is small, cysteine-rich peptide, antimicrobial peptide similar to defensins and thionins. Hepcidin (unprocessed, proprotein in mouse 83aa, rat/human 84aa) are almost exclusively produced in liver. Human hepcidin is produced from 84aa precursor, including a putative 24aa signal peptide. The secreted form of hepcidin in blood and urine is consists of C-terminal 20, 22 or 25aa residues. In humans, 20aa and 25aa appears to be the major HEPC secreted peptides with antimicrobial activities. The three secreted HEPC alternatively spliced HEPC peptides differ at the N-terminus. The link between hepcidins and iron metabolism is that hepcidin expression is abolished in mice exhibiting iron-overload due to the targeted disruption of USF2 (upstream stimulatory factor 2) gene resembling the situation in hfe-/- mice. The human gene is located at chromosome 19, in close proximity with Usf2 gene. Hepcidin levels are increased in iron loading and in beta-2 microglobulin knockout mice. Hepcidins are devoid of IRE. Like other antimicrobial peptides, hepcidin is upregulated by lipopolysaccharides (LPS).