However, in conditions characterized by the Type I interferon (IFN) gene signature (e.g., SLE, primary Sjögren’s syndrome and inflammatory myopathies), CRP appears to be an unreliable marker of inflammation, since the circulating levels of CRP can be modest—despite the presence of extensive inflammation, as evidenced by an increased level of IL-6 in the circulation [9,10]. The gene discussed is CRP; the disease is systemic lupus erythematosus.