Here, we showed increased levels of HMGB1, TLR4, NF-κB and their downstream target genes TNF-α and IL-1β in MRL/lpr mice, compared with control mice, as well as more severe inflammatory damage in kidney tissues.These results indicate the strong inflammation-mediating role of the HMGB1/TLR4/NF-κB pathway in LN. The gene discussed is NFKB1; the disease is lobular neoplasia.