MRL.Faslpr deficient in Myd88 or Tlr7 had reduced clinical disease, while those deficient in Tlr9 unexpectedly had significantly exacerbated disease, suggesting that Tlr9 suppresses development of clinical pathology in lupus [8–10] despite its paradoxical role in breaking tolerance in anti-nucleosome and anti-DNA B cells. Here, TLR7 is linked to systemic lupus erythematosus.