Currently, the role of NLRP3 inflammasome in the development of multiple types of ALI is also reported, and the main pathogenic mechanisms include the following: (1) increased permeability of alveolar epithelial and barrier dysfunction; (2) overproduction of cytokines including IL-6, IL-1β, and TNF-α; and (3) involvement of tissue remodeling and pulmonary fibrosis in the late stage of ALI [7–9]. This evidence concerns the gene IL6 and acute respiratory distress syndrome.