In CYP1A1−/− deficient mice, CYP1A1 knockout enhanced LPS-induced ALI by inducing pulmonary edema, neutrophil infiltration, and destruction of lung parenchyma; meanwhile, TNF-α, IL-1β, IL-6, and NO levels were elevated, and these impairments were mediated by the overactivation of NF-κB and iNOS (Tian et al., 2020). This evidence concerns the gene NFKB1 and acute respiratory distress syndrome.