In the absence of TLR9, autoimmune disease is exacerbated, resulting in heightened activation of lymphocytes and plasmacytoid DC, as well as elevated levels of serum IgG and IFN-α (Christensen et al. 2006), suggesting the activation of TLR9 may be potential therapeutic strategies for SLE. The gene discussed is TLR9; the disease is systemic lupus erythematosus.