The protein A20-binding inhibitor of NF-κB1 (ABIN1) is required to prevent systemic lupus erythematosus (SLE), because mutant mice expressing the functionally defective ABIN1[D485N] mutant, which cannot interact with ubiquitin chains, leads to the spontaneous development of autoimmunity (1). This evidence concerns the gene TNIP1 and systemic lupus erythematosus.