Gastric cancer is one of the most common malignancies in the world. Gastric carcinogenesis is multifactorial. Although some environmental factors, such as excessive intake of salt and N-nitroso compounds in foods, are involved in this process, Helicobacter pylori has been closely linked to an increased risk of the development of gastric adenocarcinoma. The IARC/WHO in 1994 concluded that H. pylori is a definite carcinogen in humans based on seroepidemiological evidence. H. pylori infection is associated with both intestinal and diffuse types of gastric cancer. Strong evidence has accumulated that H. pylori infection has been active in the development of gastric adenocarcinoma in the Mongolian gerbil (MG) model after long term infection and with or without treatment using low-dose chemical carcinogens. There are several criticisms of these reports. The most troublesome issue is the diagnostic criteria for gastric cancer in MGs, especially for well-differentiated cancers induced by H. pylori infection. Hence, common criteria for the diagnosis of gastric cancer in MGs is required. Another scientific approach is to find genetic-evidence to confirm the diagnosis. Such evidence could indicate directly that H. pylori infection itself is a promoter, initiator, or both in the development of gastric adenocarcinoma.