The importance of A20 in modifying NF-κB activity and immune responses was confirmed in A20-deficient mice that developed profound inflammation and cachexia, and died prematurely (117) (Table 1), and cell-specific deletion of A20 in myeloid cells, dendritic cells (DCs) or B cells, results in autoimmune phenotypes including polyarthritis and enteritis (Table 1) (121–124). This evidence concerns the gene TNFAIP3 and Cachexia.