The innate immune system plays a central role in ARDS through neutrophil priming, secretion of inflammatory mediators and activation of downstream inflammatory pathways.1 5 6 Elevated concentrations of pro-inflammatory mediators, including interleukin (IL) 1β and IL-18, are associated with worsened outcomes in ARDS, and blockade is beneficial in experimental lung injury models.7, 10 These inflammatory mediators are predominantly processed via a multimeric protein structure called the inflammasome, which consists of sensor proteins, adaptor proteins and an effector enzyme.11 Here, IL18 is linked to acute respiratory distress syndrome.