Interestingly, the presence of anti-interferon-γ autoantibodies was associated with higher clinical SLE disease activity (as measured by the SLE disease activity index, hypocomplementemia, and elevated titers of double-stranded-DNA antibody), and demonstrated increased expression of IFN-α/β-inducible genes compared to those with anti-IFNα autoantibodies and healthy controls. The gene discussed is IFNA2; the disease is systemic lupus erythematosus.