Mice deficient for A20 develop severe multiorgan inflammation [74] and tissue-specific deletion of A20 results in different phenotypes that resembles human autoimmune diseases such as inflammatory polyarthritis (macrophages), SLE (dendritic cells), IBD (intestinal epithelial cells) or psoriasis (keratinocyes) [73]. The gene discussed is TNFAIP3; the disease is inflammatory bowel disease.