Epidemiological studies have suggested that the development of gastric cancer may be attributed to hypoxia-induced reactive oxygen species (ROS) [2] and that ROS generated within the gastric mucosa are related to continuous exposure to H. pylori infection, ingested food, and cigarette smoking, etc. Accumulating data indicate that the H. pylori CagA protein, which is injected into gastric epithelial cells through T4SS, behaves as a bacterial oncoprotein [3]: CagA continuously dysregulates multiple oncogenic signaling pathways and promotes tumorigenesis [4]. The gene discussed is S100A8; the disease is gastric cancer.