To address the functional consequence of an A20 DUB inactivation in the development of autoimmunity in vivo, we generated a knock-in mouse line mutated in the deubiquitinase function of A20 by substituting the active site cysteine (C) residue with an arginine (R) (A20C103R) (Fig. 1A). This evidence concerns the gene TNFAIP3 and Autoimmunity.