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Nuclear factor-κB is a transcriptional factor required for the gene expression of many inflammatory mediators. Nuclear factor-κB activation requires removal and degradation of its inhibitor κB, an event that occurs after phosphorylation of inhibitor κB by a complex of inhibitor κB kinases. These events allow nuclear factor-κB to translocate into the nucleus, where it binds to κB elements and initiates transcription. Inappropriate and prolonged activation of nuclear factor-κB has been linked to several diseases associated with inflammatory events, including septic shock, acute respiratory distress syndrome, ischemia, and reperfusion injury. Thus, the key role of nuclear factor-κB in regulating inflammation makes this factor a therapeutic target for reducing tissue and organ damage. Regulation and control of nuclear factor-κB can be achieved by gene modification strategies or by pharmacologic inhibition of the key components of the cascade that leads to nuclear factor-κB activation. The purpose of our review is to describe these novel therapeutic approaches and their potential efficacy.