It has been known for 70 years that gastric cancer occurs mainly in a stomach with gastritis. Gastritis was previously so prevalent that it was regarded as an aging phenomenon. Since the description of Helicobacter pylori (Hp) as the main cause of gastritis and peptic ulcer disease (1), Hp was soon accepted as the most important gastric carcinogen (2). The mechanism by which Hp induces gastric cancer has not been found despite intensive research for 30 years. However, a major breakthrough was achieved when Uemura et al. (3) described that Hp predisposes to gastric cancer only when having induced atrophy of the oxyntic mucosa. This led us to propose that hypergastrinemia due to reduced acid secretion leading to gastric hypoacidity was the pathogenic factor in Hp-associated gastric cancer (4). Autoimmune gastritis (AI) has been accepted as a separate type of gastritis having a much lower prevalence than Hp gastritis. Hp and AI gastritis have special traits (Table 1), but no test that can definitively discriminate between the 2 types
