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). The gene discussed is NFKB1; the disease is acute respiratory distress syndrome.