Quantitative PCR demonstrated that exposure of EBV-infected gastric cells (NC1-N87) for 48 h to Hp increases the proliferation of the EBV-infected cells and the expression level of DNA methyltransferases (MTs), which silence the tumor suppressor genes (TSGs) controlling many pathways associated with gastric cancer (cell cycle, apoptosis, and DNA repair) [43]. The gene discussed is HP; the disease is gastric cancer.