Overexpression of type I IFN-inducible genes, known as “the IFN signature”, is a common feature of many autoimmune diseases [26, 27], including RA patients with poor clinical outcome [28–30] and systemic lupus erythematosus [31, 32], where the predominant IFN producing cells, pDCs, are reduced in number in the blood but are abundant in skin and lymph nodes [33]. The gene discussed is IFNA1; the disease is rheumatoid arthritis.