Further studies found that extracellular HMGB1 was also bound to NMDARs and formed a C1q-HMGB1-NMDARs complex on the dendrites of neurons. The complex interaction with RAGE/TLR4 on microglia led to neuronal dendrite damage and cognitive dysfunction (120). These results suggest that targeting HMGB1 in SLE is promising, but more investigations are needed. This evidence concerns the gene HMGB1 and systemic lupus erythematosus.