Indeed, the relevance of their therapeutic action is highlighted by reports that MyD88 signalling is essential for pathogenesis in the MRL/Lpr mouse,6 in particular by promoting the generation of interferon (IFN)α, IL-6 and ANAs required to drive autoimmune renal disease.6,7 Dissection of the pathogenic roles of MyD88 has indicated that deficiency solely in B cells is sufficient to protect against nephritis in both the MRL/Lpr and Lyn–/– mouse models of lupus,8,9 as MyD88 signalling is essential for ANA production, activation of nephrotoxic T cells and glomerulonephritis. The gene discussed is MYD88; the disease is nephritis.