Highly active in ARDS are pro-inflammatory mediators such as inducible Nitric Oxide Synthase (iNOS), tumor necrosis factor (TNF) and interleukin-1β (IL-1β), leading to organ-related detrimental effects in lung and vasculature (17–19), including thrombotic events (20, 21). Here, IL1B is linked to acute respiratory distress syndrome.