Data collected from tissue biopsies indicate that Ras mutation may play a role in the development of gastric cancer in human patients [50], and our data put forward the idea that enhanced tumorigenic potential created by cooperation between JNK pathway activation via the bacterial genetic factor CagA and sporadic activation of Ras in host cells could drive gastric cancer formation in a subset of H. pylori infections. This evidence concerns the gene S100A8 and gastric cancer.