Importantly, the results showed that infections performed with H. pylori(WT) and H. pylori(CagA−) without EBV did not have any direct effect on the oncogenic phenotype or on the transcript levels of the TSGs examined, indicating that H. pylori can enhance the functional ability of EBV to drive oncogenesis but is limited in its own capacity to drive the oncogenic phenotype of gastric epithelial cells (Fig. S6B and C). The gene discussed is S100A8; the disease is infection.