HAMP encodes hepcidin, a 25-amino acid peptide hormone that serves as the master regulator of systemic iron homeostasis 1. Hepcidin functions by binding to ferroportin, the cellular iron exporter, causing its internalization and degradation, which decreases cellular iron export and completes a homeostatic feedback loop where iron levels regulate hepcidin secretion 2. This hormone is primarily produced by hepatocytes and macrophages and controls iron efflux throughout the body, regulating intestinal iron absorption and maternal-fetal iron transport 3. Beyond iron regulation, hepcidin also functions as a mediator of innate immunity and is responsible for hypoferremia during inflammation 3. Disruption of hepcidin function is central to hemochromatosis pathogenesis, where genetically determined lack of hepcidin synthesis or activity causes iron overload, similar to insulin's role in diabetes 4. HAMP mutations are associated with non-HFE hemochromatosis, particularly hemochromatosis 2B, which can present with earlier onset and more severe phenotypes than classic hemochromatosis 5. The gene's polymorphisms, such as rs10421768, can influence hepcidin levels and may affect disease susceptibility 6.