Chronic inflammation caused by infection, autoimmunity or exposure to irritants, contributes to tumor promotion and progression. Many of the tumor-promoting effects of inflammation depend on the activation of NF-kB dependent genes encoding cytokines, growth factors, survival proteins and others. Interference with NF-kB signalling therefore represents a potential new therapeutic approach. An important regulator of inflammatory signalling is the ubiquitin-editing protein A20, which acts as a break on excessive NF-kB activation. Through conditional A20 ablation in different mouse tissues, we aim to establish the cell-specific role of A20 in the control over excessive inflammation and inflammation induced cancer.