The previous work has revealed that H. pylori virulence factor CagA contributed to gastric carcinoma cells invasiveness through upregulating CDX2-mediated Claudin-2 expression in AGS gastric cancer cells, thereby disrupting tight junction [6], and H. pylori promoted CDX2-mediated IM through NF-κB [7], SOX2 [8] and Activin A receptor type I (ACVR1) [3]. Here, S100A8 is linked to gastric cancer.