To clarify the interactions between EBV infection and host abnormalities in the stomach mucosa at different phases of carcinogenesis of EBVaGC, the following questions were investigated: 1) whether lost ARID1A coexists with EBV infection in non-neoplastic glands; 2) whether lost ARID1A affects the pathology of EBVaGC within the proper mucosal layer; and 3) whether lost ARID1A promotes the EBV infection of stomach epithelial cells. This evidence concerns the gene ARID1A and Epstein-Barr virus infection.