S100A8 and gastric cancer: In addition, although it has been shown that H. pylori primarily relies on CagA for its virulence in the development of GC (10, 51, 52), and EBV can induce gastric mucosal lesions through the hypermethylation of CpG islands in the promoter regions of various cancer-associated genes (53), it is still largely unclear how the co-infection of H. pylori with EBV induces GCs.