A previous study showed that brevilin A could bind with the inhibitor of κB kinase α/β to inhibit its phosphorylation, reduce the activation of the NF-κB pathway in macrophages induced by LPS/IFN-γ in a dose-dependent manner, decrease the expression of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α in macrophages, and effectively alleviate inflammatory reaction and lung tissue injury in ALI/ARDS [59]. This evidence concerns the gene IL6 and acute respiratory distress syndrome.