Inflammation is a self-limiting response to infection and injury, and is essential both to limit damage and to promote repair. Excessive or sustained inflammation leads to extensive tissue damage and to the development and progression of several diseases with a huge social impact, including septic shock, autoimmune diseases and cancer. Inflammatory responses involve rapid changes in gene expression that take place both in professional inflammatory cells and in tissue cells exposed to the inflammatory stimulus. Multiple steps of inflammation, from microbial killing to endothelial activation and cell migration, are regulated by the transcription factors of the NF-?B family, which co-ordinately control hundreds of genes Its mechanistic understanding requires that NF-kB-driven transcription is understood not only qualitatively but quantitatively. Our group is performing quantitative time-resolved assays on single living cells or cell populations to collect unambiguous and repeatable measurements. These measurements will be used to generate predictive mathematical models for a deeper understanding of the NF-kB -dependent transcriptional network in inflammation and cancer.