Mice with an A20 deletion in CD11c+ DCs (Tnfaip3flox/flox Cd11c-Cre+ mice) rapidly develop a significantly disordered immune homeostasis, and showed various phenotypes, such as inflammatory bowel disease, systemic autoimmunity resembling SLE, and multiorgan inflammation (4, 8–10). The gene discussed is TNFAIP3; the disease is inflammatory bowel disease.