Liao et al. [22] found that in the preterm baboon BPD model induced by hyperoxia, targeted deletion of NLRP3 could restrain Caspase-1 activity, significantly downregulate the expression of IL-1β and IL-18, significantly reduce the incidence of cell death, and protect preterm baboons from hyperoxia-induced inflammation, as well as abnormal alveolar simplification. The gene discussed is NLRP3; the disease is bronchopulmonary dysplasia.