Considering that activation of NLRP3 and secretion of IL-1β and IL-18 in alveolar macrophages contribute to pulmonary inflammation and injury [23], and that there is a known relationship between leptin, IL-18 serum levels, lung function, and body fat [30], further studies should be conducted to investigate the role of this adipokine in promoting maturation of NLRP3-derived pro-inflammatory cytokines in the context of obesity-associated pulmonary diseases. This evidence concerns the gene LEP and lung disorder.