HAMP, encoding hepcidin antimicrobial peptide, is a key gene in regulating systemic iron homeostasis. Hepcidin, as a peptide hormone, binds to ferroportin, an iron exporter, leading to its internalization and degradation, thus controlling cellular iron efflux. This regulation forms a homeostatic loop where iron levels regulate hepcidin secretion, which in turn manages ferroportin levels on the cell surface [4,6].

In disease research, HAMP shows potential as a biomarker. In gastric cancer, high HAMP expression is correlated 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, HAMP promotes cell proliferation, invasion, and migration by activating the NF-κB pathway, and non-coding RNAs can regulate HAMP [2]. In hepatocellular carcinoma, HAMP has a better ability to diagnose the disease and predict PD1 treatment sensitivity, and is positively correlated with immune cell infiltration and immune checkpoint expression [3]. In type 2 diabetes, differences in DNA methylation of HAMP in blood cells may predict disease development [7]. Mutations in HAMP can also cause atypical juvenile hereditary hemochromatosis, which may be misdiagnosed as type 1 diabetes [5].

In conclusion, HAMP is crucial for maintaining iron homeostasis. Research on HAMP using various models has revealed its significant roles in multiple diseases, such as cancer and diabetes-related conditions. Understanding HAMP's functions not only deepens our knowledge of iron metabolism but also provides potential biomarkers and therapeutic targets for these diseases.