Secretion of IFN-I is critical to antiviral defense: signaling downstream of the ubiquitous IFN-α/β receptor results in the induction of antiviral programs, collectively known as the ‘interferon signature.’ The aberrant activation of the IFN pathway is a hallmark of several autoimmune diseases, as exemplified by systemic lupus erythematosus (3, 4). This evidence concerns the gene IFNA1 and systemic lupus erythematosus.