A possible pathogenetic mechanism involves the persistent H. pylori colonization and inflammation of the gastric mucosa, particularly when the H. pylori strains express the cytoxin-associated gene (CagA) which often results in the development of chronic atrophic gastritis and subsequently hypergastrinemia, through a reverse-feedback mechanism; hypergastrinemia is considered to be a possible risk factor for the development of colorectal cancer [3-5]. The gene discussed is S100A8; the disease is chronic atrophic gastritis.