The International Agency of Research on Cancer, sponsored by the World Health Organization, has categorized Helicobacter pylori infection as a class I carcinogen and a definite cause of human gastric cancer. This decision was made largely on the basis of epidemiological evidence relating infection with H. pylori to the aetiology of gastric carcinoma and gastric lymphoma. Epidemiological studies suggest that at least 30% of gastric cancers in the developed world and 50% of those in the developing world may be attributed to H. pylori (although these figures might be as high as 75% and 90% respectively). Prevention of these cancers would result in a considerable saving in terms of morbidity, mortality and health service resources. A strategy of screening populations in middle age and treating those infected could be relatively inexpensive to administer but the efficacy is totally unknown and requires evaluation in a randomized controlled trial. Studies designed to address this issue in the general population would need to be large and long-term if gastric cancer is used as an end-point. With respect to carcinogenic mechanisms, H. pylori affects several aspects of gastric epithelial cell function that may be related to cancer. Notably, cell proliferation is significantly elevated, thus increasing the likelihood of unrepaired genetic lesions and DNA mutations.