The studies by Cárdenas-Mondragón et co-workers give evidence of this mechanism; in pediatrics patients they demonstrated that co-infection with EBV and H. pylori CagA+ is more associated with severe gastritis than cases with single H. pylori CagA+ infection [52], as well as the study with Latin American patients confirm that EBV co-participates with H. pylori to induce severe inflammation and increase the risk of progression to intestinal-type GC [53]. This evidence concerns the gene S100A8 and gastric cancer.