For decades clinicians the world over took it for granted that bacteria could not live and grow in the stomach because of the acid pH of its lumen. It was, therefore, a great surprise when Barry Marshall and Robin Warren reported in The Lancet 1 in 1984 that bacteria resembling campylobacter could be found beneath the gastric mucus layer that lines the surface epithelium of the stomach, and that their presence was associated with gastritis, and gastric and duodenal ulcers. In fact, the same authors had already reported their fi nding of “unidentifi ed curved bacilli on gastric epithelium in active chronic gastritis”, which they set out a year earlier in two letters to The Lancet. 2,3 Indeed, similar bacteria had been described repeatedly during the previous century, but had been overlooked partly because they could not be seen with conventional stains. In the 4 years following Marshall and Warren’s report, it was established that Campylobacter pylori infection caused an acute histological gastritis that could become chronic, that it was the causative agent in type-B gastritis, that it was often found in patients with peptic ulcer disease, and that the eradication of the organism was associated with the healing of gastritis and a lower relapse rate in duodenal ulcer disease. 4 The idea that peptic ulcer disease was related to gastric hypersecretion, stress, smoking, or alcohol was abandoned, and the dictum “no acid, no ulcer” was replaced with “no bacterium, no ulcer”. By 1993 (10 years after the fi rst report) it had been shown that half of the world’s population were infected with C pylori, that the mode of transmission was probably fecal–oral, and that its prevalence increased with age and was higher in lower socioeconomic groups. Infection with C pylori could be diagnosed using serology, breath testing, biopsy, and culture. Eff ective therapies had been established, and many double-blind trials had shown that eradicating the bacterium, by then known as Helicobacter pylori, usually cured duodenal ulcer disease. These were signifi cant achievements, but of even greater importance from a biological viewpoint was the link between H pylori and cancer. Before Marshall and Warren’s discovery, no factors had been shown to be causally linked with gastric cancer, although a link between several types of food and drink and gastric cancer had been tentatively suggested. Pivotal work demonstrated that H pylori was related to gastric malignancies, 5 and further studies led the International