Dnase1L3 knockout mice show increased production of extrafollicular PCs and develop SLE; however, when these mice were crossed with IFNα receptor (IFNαR)-knockout mice, their symptoms improved, suggesting a complex interplay involving TLR9, IFNα, and PC differentiation in the context of autoimmune diseases (22). This evidence concerns the gene TLR9 and systemic lupus erythematosus.