After TLR4 recognition by extracellular HMGB1, AP-1 and IRF3/5/7 are upregulated and promote the transfer of NF-κB to regulate the expression of genes encoding inflammatory cytokines through the TLR4 adapter MyD88 and TRIF [23–25].TLR4 is involved in autoimmunity and LN, as well as NF-κB activity is essential for immune cell activation [26–28]. This evidence concerns the gene TLR4 and lobular neoplasia.