Hamp, encoding hepcidin antimicrobial peptide, is crucial for regulating systemic iron homeostasis. Hepcidin binds to ferroportin, an iron exporter on various cell surfaces, inducing its internalization and degradation, thus controlling cellular iron efflux. This process is part of the homeostatic loop where iron regulates hepcidin secretion, which in turn manages ferroportin levels [4,6].

In gastric cancer, high HAMP expression is associated with poor overall survival and is related to immune cell infiltration levels, suggesting it may serve as an independent prognostic biomarker through the immune pathway [1]. In non-small cell lung cancer (NSCLC), HAMP promotes cell proliferation, invasion, and migration by activating the NF-κB pathway, and non-coding RNAs can regulate HAMP [2]. In hepatocellular carcinoma (HCC), HAMP shows potential as a diagnostic, PD-(L)1 immunotherapy sensitivity, and prognostic biomarker [3]. In addition, loss-of-function mutations in HAMP can lead to atypical juvenile hereditary hemochromatosis presenting as diabetes with positive pancreatic islet autoantibodies [5].

In conclusion, Hamp plays a vital role in iron metabolism. Studies on Hamp in various disease models, such as those of gastric cancer, NSCLC, HCC, and juvenile hereditary hemochromatosis, have revealed its significance in disease prognosis, diagnosis, and as a potential therapeutic target, contributing to a better understanding of these disease mechanisms.