These results are consistent with autoimmunity in ABIN1[D485N] mice being driven by hyperactivation of the MyD88 signaling network and raise the possibility that small molecule inhibitors of IRAK4 and/or IRAK1 prevent (and perhaps reverse) autoimmune diseases in which alterations in the TNIP1 gene encoding ABIN1 (Introduction) or other genes causing hyperactivation of MyD88 signaling are a contributory factor. This evidence concerns the gene IRAK4 and autoimmune disease.