Multiple studies have confirmed the involvement of TLR signaling, in particular MyD88-dependent TLRs and endosomal TLR7 and TLR9, in autoreactive B cell activation and germinal center (GC) formation (19), autoantibody production (20, 21), and development of autoantibody-related pathologies such as glomerulonephritis in the context of the human disease systemic lupus erythematosus (SLE) (22, 23) and in models using the lupus-prone mouse strain MRL/lpr (24). The gene discussed is TLR7; the disease is systemic lupus erythematosus.