In this study, through survival analysis in different samples and multifarious experiments, an important mechanism is identified in the stemness of gastric adenocarcinoma: the deficiency of ATOH1‐regulated by its DNMT1 level blocks GAS1 promoter transcription, further activating the RET/AKT/mTOR pathway and promoting CSC‐like qualities and chemotherapy resistance, and hence presents a significant association with the poor prognosis. This evidence concerns the gene GAS1 and gastric adenocarcinoma.