In Tlr7-deficient mouse models of SLE, disease is ameliorated due to diminished anti-RNA autoantibody levels and suppressed nephritis development.9 However, Tlr7 deficiency does not affect anti-dsDNA autoantibody development, which is TLR9 dependent.9 Moreover, studies in both humans with SLE and mouse models of SLE have shown that IFNα also contributes to the immunopathogenesis of this disease.32–34 Unlike SLE, T1D is an organ-specific autoimmune disorder mediated mostly by autoreactive T cells. The gene discussed is TLR9; the disease is systemic lupus erythematosus.