In the present study, we demonstrated the following: 1) lost ARID1A coexisted with EBV-infected cells in non-neoplastic epithelial cells showing degenerative glands; 2) lost ARID1A correlated with morphological features (tubular structure) of EBVaGC in the proper mucosal layer; and 3) lost ARID1A promoted the infection of EBV in stomach epithelial cells, indicating that lost ARID1A induces permissive conditions for EBV infection, thereby initiating the viral-driven carcinogenesis. Here, ARID1A is linked to Epstein-Barr virus infection.