S100A8 and gastric cancer: Therefore, it is necessary to confirm that (i) the role of H. pylori-mediated upregulation of IL-22 in gastric cancer cells, (ii) the activation of STAT3 dependent on H. pylori-mediated IL-22 and/or H. pylori CagA, (iii) the role of CagA in H. pylori-mediated upregulation of IL-22.