The role of the immune system in patients with acute respiratory distress syndrome (ARDS) and ALI is well known; briefly, soon after lung injury, endothelial cells are damaged with gap formation that allows fluid permeability, activation, and migration of neutrophils with activation of pro-inflammatory cytokines such as TNF-α, IL-1β, and the transcriptional regulatory NF-κB. Here, IL1B is linked to acute respiratory distress syndrome.