CGAS and gastric cancer: It mainly presents with moderately‐ to poorly‐differentiated adenocarcinoma and harbors intense infiltration of lymphocytes.[34] The EB virus has been demonstrated to induce oncogenesis in gastric epithelial cells by activating various cancer‐promoting signaling pathways, including Wnt, Akt/mTOR, cGAS/STING, and JAK2/STAT1 pathways.[35, 36, 37, 38] We supposed that for EBV‐positive GC, EBV might activate the mTOR‐eIF4E pathway to different extents.