In gastric colonization by Helicobacter pylori, the frequency of apoptosis, a natural programmed death of a cell, increases from 2-3 to 16% (mean 8%). One of pathogenic pathways of apoptosis in the mucosa of the gastrointestinal tract is an extracellular pathway, called a receptive pathway, in which Fas receptors and an epidermal growth factor receptor (EGFR) get activated. Another pathogenic pathway is an intracellular pathway, called a mitochondrial pathway, in which mitochondrial proteins from the Bcl-2 family get activated or inhibited. The studies proved that H. pylori induced apoptosis of gastric mucosa via: cag A pathogenicity island, urease, lipopolisaccharide (LPS), cytotoxin Vac A as well as monochloramine and nitrogen oxide. A process of apoptosis induced by H. pylori results in chronic gastritis and ulcer disease, whereas inhibition of apoptosis and induction of proliferation is related to the development of a cancerous process.