This pathological condition is caused by the overactivation of innate immune cells in the lung, mostly alveolar macrophages, which play a pivotal role in ARDS onset causing an over-release of proinflammatory cytokines (IL-6, TNF-α, IL-1β) as a consequence of NLRP3 activation [21,22,23]. Here, IL1B is linked to acute respiratory distress syndrome.