We used cholecystokinin (CCK) to stimulate acinar cells to establish a pancreatitis cell model, as previously reported.[19] We found that AKT/mTOR/ribosomal protein S6 (RPS6)/eukaryotic translation initiation factor 4E‐binding protein 1 (4EBP1) signaling was activated in GSDMD‐knockout acinar cells but was inhibited in GSDMD‐overexpressing (GSDMD‐OE) acinar cells (Figure 4E–H). The gene discussed is MTOR; the disease is pancreatitis.