The biological model of gastric carcinogenesis can be described as a series of sequential phases. The first consists of a chronic active inflammatory response to Helicobacter pylori infection. Infiltration of the gastric mucosa by mucosa-associated lymphoid tissue and polymorphonuclear neutrophils, as well as damage to the epithelial cells, characterize this phase. The second phase is dominated by alterations of the epithelial cell cycle, especially increased rates of apoptosis and cell proliferation. These changes may be responsible for the multifocal atrophy that characterizes the type of gastritis associated with an increased risk of cancer. The third, more advanced phase of the model displays nuclear and architectural abnormalities, which may represent progressive mutational events as expected in classical molecular models of carcinogenesis. The importance of a comprehensive view of the biological model is stressed.