As a recognized risk factor of GC, infection of Helicobacter pylori (H. pylori) contributes to the generation of ROS by cytotoxin-associated gene A (CagA) [6], subsequently activating Wnt, Ras, and mechanistic targets of rapamycin (mTOR) to drive the initiation of gastric carcinogenesis [7–10]. This evidence concerns the gene MTOR and infection.