In conclusion, the results of this study confirm a wide overexpression of TLR3, TLR7, and TLR9 in kidney sections of LN patients and demonstrate a correlation with clinical and histological indices, further supporting a putative role for these mediators of innate immune response in the pathogenesis of lupus nephritis and suggesting them as potential therapeutic target. The gene discussed is TLR3; the disease is lobular neoplasia.