The infection caused by H. pylori triggers the upregulation of fibroblast activating protein (FAP) and fibroblast surface protein (FSP) mRNA, as well as elevated levels of pro-inflammatory factors such as IL-6, IL-8, COX-2, and SDF-1. Overexpression of FAP hinders the regulation of fibroblast growth, obstructs tissue repair, and promotes the progression of epithelial-mesenchymal transition (EMT) and the development of gastric cancer. Here, CXCL1 is linked to infection.