The actions of TNF-α in the pathogenesis of lupus nephritis have also been confounded by reports that anti-TNF-α treatment in NZB/W mice with active lupus nephritis induced by IFN-α protected the mice against renal damage and prolonged their survival by attenuating the kidney's response to glomerular immune complex deposition [71]. The gene discussed is IFNA1; the disease is lupus nephritis.