IFNA1 and glomerulonephritis: Indeed, treatment using the JAK2-selective inhibitor CEP-33779 in both NZB/W F1 and MRLlpr/lpr mice saw dose-dependent improvements in lymphadenopathy and splenomegaly, reductions in systemic C3 and proinflammatory cytokines, including IL-1, IL-12, IFN-α, IL-17A, and TNF-α, reductions in autoantibody-producing plasma cells, increased survival, and significant improvements in glomerulonephritis through blockade of STAT3-mediated signaling (184, 185).