It is noteworthy that while gastric cancer cells undergoing chemotherapy, radiotherapy, or other stress responses often experience cell damage or apoptosis, leading to the release of endogenous dsDNA into the cytoplasm and activating anti-tumor immune responses via the cGAS-STING pathway, these cells may also evade this immune surveillance through various mechanisms, such as reducing their DNA sensing function. This evidence concerns the gene STING1 and neoplasm.