Gastric carcinoma is the world's overall second most common cancer. Besides obvious environmental factors, recent epidemiological studies and a better knowledge of Helicobacter Pylori biological properties revealed that the microorganism is involved in the first steps of gastric carcinogenesis as proposed by the Correa model (from normal gastric tissue through superficial gastritis, multifocal atrophic gastritis, intestinal metaplasia and dysplasia to carcinoma). Significant correlation between the prevalence of H. pylori infection and incidence of gastric carcinoma (mainly the intestinal type) in various geographical areas has been reported. The high prevalence of HP in pre-neoplastic states and in cases of early gastric cancer indicates the infection would precede the development of gastric cancer. HP-related chronic inflammation of gastric mucosa with increased mucosal cell proliferation, deficit in local ascorbic acid concentration, topical ammonia toxicity are putative mechanisms that overexpose a weakened gastric mucosa to environmental carcinogens.