The main findings included the following: (1) the STING C-176 inhibitor significantly reduced lung injury and pulmonary fibrosis after intestinal ischemia–reperfusion injury; (2) the STING C-176 inhibitor significantly ameliorated pulmonary apoptosis and pyroptosis; and (3) the protective effects of C-176 against ALI after intestinal ischemia–reperfusion injury may be associated with STING–AMPK signaling. The gene discussed is STING1; the disease is acute respiratory distress syndrome.