In line with the Song et al. study showed that infection with H. pylori is well recognized as a kind of genotoxic DNA pathogens to trigger STING signaling, including IRF3 phosphorylation [49], we found that phosphorylation and nuclear translocation of IRF3 was increased in gastric epithelial cells in response to H. pylori stimulation, which was attributed to activation of cGAS-STING pathway, including phosphorylation of TBK and STING. The gene discussed is STING1; the disease is infection.