In another lupus-prone mice, Lyn−/− mice, inhibition of IL-6 trans-signaling by sgp130Fc exerted relatively little effect on abnormal immune processes along with unchanged pathogenic autoantibodies and renal immune complexes deposition, whereas sgp130Fc indeed ameliorated glomerulonephritis and preserved renal function by hampering complement fixation, leukocytes infiltration, and macrophage expansion in this model (134). The gene discussed is IL6; the disease is glomerulonephritis.