MRLlpr/lpr lupus-prone mice that are genetically deficient in TLR7, TLR9, both TLR7 and TLR9, or myeloid differentiation primary response 88 (MyD88) showed that although TLR7 and TLR9 acted in parallel pathways on different subsets of autoantibodies, TLR9 suppressed the production of TLR7-dependent RNA-associated autoantibodies [24], and they mentioned that TLR- and MyD88-independent components are required for the induction of SLE in MRLlpr mice [24]. Here, TLR9 is linked to systemic lupus erythematosus.