In patients with EBV-positive GC, both the host and viral genomes exhibit more extensive CpG methylation than in patients with EBV-negative GC.96 In addition to epigenetic alterations, somatic mutations in TP53, KRAS, ARID1A, PIK3CA, BCOR, and PD-L1 are present in GC cells.97 The EBV of GCs generally exhibits restricted expression of latent genes (latency type I), but involvement of LMP2A has also been suggested.98 Histologically, infiltrations of lymphocytes are typically found in EBV-positive epithelial cancers, GC, and NPC. This evidence concerns the gene ARID1A and nasopharyngeal carcinoma.