Studies in humans showed neutrophil inflammasome activation secondary to SARS-CoV-2 infection, with increased ASC speck formation, IL-1β and IL-18 production, and pyroptosis, all associated with worsened disease severity.53 54 Similarly, work by both Leal et al and Aymonnier et al found the neutrophil inflammasome to be the predominant source of IL-1β in SARS-CoV-2-associated ARDS in humans.55 56 The human NLRP3 inflammasome also appears to be activated by influenza viruses in multiple immune and non-immune cells.57 The gene discussed is IL18; the disease is acute respiratory distress syndrome.