Although the precise pathogenetic role of H. pylori in gastric carcinogenesis remains unclear, it has been clarified that this organism contributes to modifications in epithelial cell proliferation, which may be the initiating event in a cascade culminating in the development of gastric cancer [9], but it is not known whether the increased risk is due to the presence of mutant p53 generated by chronic gastritis or to a direct action of the bacteria on the p53 oncogene [10,11]. Here, TP53 is linked to gastric cancer.