Most people with stomachs colonised byHelicobacter pylori do not develop peptic ulceration, gastric adenocarcinoma or gastric lymphoma in their lifetime. Development of disease is likely to be determined by a combination of factors: the virulence of the infectingH pylori strain, the susceptibility of the host and environmental co-factors. The best studied of these disease determinants is strain virulence, and the two most studied virulence markers are expression of vacuolating cytotoxin activity and production of a non-toxigenic protein of unknown function called CagA.1 Colonisation with CagA+ strains ofH pylori is easy to detect as CagA provokes a strong systemic antibody response in the human host. In Europe and the USA, more than 60% of those colonised by H pylori have antibodies to CagA: these people have more intense gastric inflammation than those colonised by CagA−H pylori alone and are more likely to develop peptic ulcers and distal gastric adenocarcinoma.1However, most people colonised by CagA+ strains do not develop these conditions and it may be more useful to regard CagA− strains as having reduced pathogenicity than to regard CagA+ strains as pathogenic. In Japan, where Maeda et al’s study (see page 336) was conducted, not only is H pylori colonisation more prevalent than in the West, but also colonisation by CagA− strains is rare.2 …