TNIP1 and systemic lupus erythematosus: SLE was also prevented by crossing ABIN1[D485N] mice to knock-in mice expressing kinase-inactive mutants of IRAK1 or IRAK4.58 ABIN1 polymorphisms have been shown to predispose to lupus, psoriasis and other autoimmune diseases in eight human populations (see Nanda et al.58 for more information), suggesting that drugs inhibiting IRAK1 and/or IRAK4 could have therapeutic potential for the prevention and perhaps the treatment of lupus caused by hyperactivation of the MyD88 signalling network.