For example, A20 has been identified as a negative regulator of the core cross-talk element TRAF6 [75], and several studies have shown that deficiencies in A20 are associated with some autoimmune diseases, including rheumatoid arthritis [76], systemic lupus erythematosus [77], and Crohn's disease [78]. This evidence concerns the gene TNFAIP3 and Crohn disease.