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). This evidence concerns the gene ITGAX and systemic lupus erythematosus.