In conclusion, our results suggest that in situ LN cellular and molecular irregularities characterized by i) sustained type I IFN signaling, ii) potent inflammatory signals (e.g., IL-21 and chemokines like CXCL9-CXCL11) iii) impaired generation of PD1hiCD57hiGATA3hi TFH cells and IL4-signaling and iv) accumulation of extrafollicular, potentially autoreactive, ABCs, could play an important role for the loose of tolerance and the generation of autoantibodies in SLE. The gene discussed is CXCL11; the disease is systemic lupus erythematosus.