The nuclear factor kappaB family of inducible transcription factors regulates the expression of many genes. Nuclear factor kappaB has been implicated in autoimmune and inflammatory diseases, infection, cell survival, and cell transformation with subsequent promotion of cancer. In this review, we summarize features of nuclear factor kappaB regulation in several catabolic disorders, and describe its role in normal cellular function as well as provide an important link to the role of scaffold proteins, cellular receptors, and other cell signaling pathway kinases that converge on the nuclear factor kappaB signaling cascade. Subsequently, we focus on the role of nuclear factor kappaB in cell survival and oxidative stress. Finally, potential therapeutic strategies are discussed that may modify nuclear factor kappaB activity including endogenous antioxidant systems and the Fas/FasL system. However, challenges still remain in developing new therapeutic strategies that not only include identifying novel agents, but also by improving clinical endpoint definitions and by defining biological efficacy. (C) 2002 Lippincott Williams Wilkins.