Although cagA-positive H. pylori-associated human gastric cancers frequently coexist with precancerous chronic atrophic gastritis,162 the gastrointestinal neoplasms that developed in the WT cagA-Tg mice, as well as the hyperplasia shown in the cagA-Tg zebrafish did not show any overt inflammation.157,160,161 These observations are consistent with the notion that the CagA protein per se is not a potent inflammogen163–165 and indicate that inflammation is not necessarily required for the oncogenesis evoked by CagA in vivo. Here, S100A8 is linked to gastric cancer.