Deregulation of bcl-2 may function as a survival mechanism in cancer cells, predisposed to cell death. Aberrant Bcl-2 expression is a frequent occurrence in chronic atrophic gastritis, gastric epithelial dysplasia and gastric cancer. Inhibition of apoptosis through Bcl-2 expression appears to be specifically associated with promotion of gastric adenocarcinoma. In addition, loss of heterozygosity of the bcl-2 gene is a common event in well-differentiated adenocarcinoma, whereas overexpression of bcl-2 gene is observed in poorly differentiated adenocarcinoma. Bax, a homologue of Bcl-2, counters the death repressor activity of Bcl-2. In our study Bax immunostaining in gastric cancer tissue is not significantly correlated with tumor histology. Possible gene therapy using bax gene is discussed.