The importance of IL-6 in the pathogenesis of lupus nephritis has been highlighted by independent researchers who demonstrated that IL-6 can exacerbate glomerulonephritis and disease manifestations in NZB/W mice, whereas interruption of IL-6 signaling is associated with reduced circulating anti-dsDNA antibody levels, improved renal histology and function, decreased proteinuria, and increased survival in lupus-prone mice [21, 54–57]. Here, IL6 is linked to glomerulonephritis.