As a major participant in II/R-ALI, NLRP3 becomes activated following II/R and aggregates with ASC (the adaptor protein in the NLRP3 inflammasome), which co-activate caspase-1 and promote the conversion of pro-IL-1β and pro-IL-18 into IL-1β and IL-18, causing acute inflammatory response and oxidative stress in lung tissue, leading to ALI (53). This evidence concerns the gene IL1B and acute respiratory distress syndrome.