Lactoferrin is a protein involved in a large variety of activities in mammals, all of which provide protective effects for the host. Lactoferrin is abundant in the secondary granules of neutrophils; in QX 314 bromide biological fluids such as milk, tears, saliva, seminal plasma; and also in the secretions of nasal, pancreatic, gastrointestinal, bronchial, and uterine tissues. Additionally, lactoferrin has a suppressive function in a variety of tumors. In our previous study, we found that lactoferrin is significantly down-regulated in specimens of nasopharyngeal carcinoma and, in patients with NPC, is negatively associated with tumor progression, metastasis, and prognosis. Lactoferrin inhibits NPC cell proliferation, induces cell cycle arrest at G1/S phase, and inhibits both MAPK and AKT signaling. The exact mechanism by which lactoferrin inhibits cancer development is unclear. We hypothesized that such activity might be related to its anti-inflammatory function. Inflammatory responses play important roles at different stages of tumor development including initiation, promotion, invasion, and metastasis. During inflammation, levels of lactoferrin in biological fluids and epithelial cells increase dramatically. Unlike many other molecular entities associated with inflammatory responses, lactoferrin displays a modulatory role by up-regulating or downregulating inflammatory responses, depending on the status of the host and the inflammation environment. Most studies concerning lactoferrin��s anti-inflammatory response have been conducted in vitro. There is, however, a Lactoferrin knockout mouse model that was generated by Ward et al.. Those authors reported that no overt phenotypic abnormalities are found in Lactoferrin knockout mice maintained under normal physiological conditions, which Radicicol implies that lactoferrin functions redundantly with other molecules such as transferrin in vivo. To investigate the role of Lactoferrin in vivo, Ward et al. constructed the first Lactoferrin knockout mice and reported that no overt phenotypic abnormalities are observed under normal physiological conditions. They also reported that lactoferrin is a positive modulator of the neutrophil oxidative burst in response to phorbol myristate-13-acetate stimulation. Using the same model, Velliyagounder��s group reported that Lactoferrin knockout mice have higher levels of alveolar bone loss, with increased expression of proinflammatory cytokines as well as chemokines during oral infection with Aggregatibacter. actinomycetemcomitans.