H. pylori is now recognized as one of the most common pathogens afflicting humans, correlated with socioeconomic status and age. In the developed world H. pylori is believed to affect about 50% of people. H. pylori infection was found to be correlated with precancerous lesions, such as chronic atrophic gastritis in the stomach. A long time colonization of human stomach by H. pylori may lead to peptic ulcers, non-Hodgkins lymphoma of the stomach, gastric atrophy and distal gastric adenocarcinoma. Balance between proliferation and apoptosis is the essential element in maintaining the integrity of gastric mucosa. The disturbance of this balance could result in either cell loss with mucosal damage and ulcer formation or cell accumulation leading to cancer development. H. pylori has a colonization range restricted to gastric mucosa and produces a number of protein products including urease, cytotoxin, flagella, CagA, VacA, heat shock proteins and adherence factors that contribute to its ability to colonize, to avoid host defenses, and to inflict damage to the host. For example, strains that possess CagA or HspB are associated with increased severity of gastritis and with additional risk to develop atrophic gastritis and cancer, instead strains that possess VacA increase the apoptotic events in the gastric mucosa. To know the exact cascade of events activated after H. pylori infection by these proteins, may help to develop new strategies to fight, or rather to prevent, gastric cancer and other common malignancies.