Furthermore, using a H. pylori-EBV coinfection model with human gastric epithelial cells, Pandey et al. demonstrated that the epigenetic status of EBV-infected cells was modulated by the CagA-positive H. pylori infection, leading to upregulation of DNMTs and thus to promoter methylation of CpG-rich islands of cell cycle-, DNA repair, and apoptosis-related TSGs [143]. This evidence concerns the gene S100A8 and coinfection.