In summary, we report new findings that the natural product, brevilin A, covalently binds to IKKα/β, thereby inhibiting IKKα/β-mediated activation of NF-κB signaling, therefore reducing LPS/IFNγ- or TNFα/IFNγ-induced inflammation in vitro and protecting mice against LPS-induced ALI in vivo (Figure 7). This evidence concerns the gene IFNG and acute respiratory distress syndrome.