Differences in individual inflammatory response by either genetic and/or environmental effect, such as a predisposing loss of ARID1A in epithelial cells before EBV infection [118] or single nucleotide polymorphisms of promoter region of interleukin-10 and/or tumor necrosis factor-α [119], possibly affect the oncogenic pathway to EBVaGC. This evidence concerns the gene ARID1A and Epstein-Barr virus infection.