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The transcription factor nuclear factor-κB (NF-κB) is critical for the inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules. The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-κB, which further explains the mechanism of action of these drugs. This inhibition prevented the degradation of the NF-κB inhibitor, IκB, and therefore NF-κB was retained in the cytosol. Sodium salicylate and aspirin also inhibited NF-κB-dependent transcription from the Igκ enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells.