It has been reported that loss of TFF1 expression in TFF1‐knockout (KO) (TFF1∆/∆) mice promotes STAT3 activation and leads to a proinflammatory phenotype that includes spontaneous development of adenocarcinomas.[13] We then generated gastric organoids from 20 months old TFF1∆/∆ mice and the counterpart wild type (WT) mice and found that the organoids from TFF1∆/∆ mice had significantly increased protein levels of p‐STAT3 and NAT10 (Figure 4L). The gene discussed is TFF1; the disease is adenocarcinoma.