In a mouse model of intestinal ischemia-reperfusion-induced ALI, complement C5a activated alveolar macrophages and bound to its surface C5a receptor, leading to the upregulation of LC-11 in alveolar macrophages, alveolar macrophage autophagy, and apoptosis, thus disrupting the lung dynamic equilibrium, and promoting the development of ALI/ARDS, while the injection of autophagy inhibitor 3-MA or knockdown of autophagy protein ATG5 in mice suppressed alveolar macrophage autophagy, inhibited macrophage apoptosis, and reduced the degree of lung injury (126). The gene discussed is ATG5; the disease is acute respiratory distress syndrome.