S100A8 and gastric cancer: H. pylori could colonize gastric epithelial cells due to its main components enabling it to survive in an acidic stomach environment and attach to host cells through the interaction of microbial adhesins with host cell receptors through flagellate-mediated motility; its virulence factors such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA), are implicated in the development of GC [6, 7].