Around one week later, partial patients exhibited difficulty breathing and hypoxia, during which the secretion of intracellular pro-inflammatory factors IL-6, IL-17 and TNF-α increased significantly, and the total number of circulating lymphocytes decreased [55,56], which rapidly deteriorated into acute respiratory distress syndrome (ARDS) [57], sepsis, blood coagulation dysfunction and irreversible metabolic acidosis [58], eventually some severe cases would lead to death. The gene discussed is TNF; the disease is acute respiratory distress syndrome.