Given their central role as transcriptional regulators of type I Interferon (IFN-α and -β) biology, they have been implicated in in the pathology of several autoimmune and autoinflammatory conditions, including systemic lupus erythematosus (SLE) in which overexpression of type I IFNs is thought to be a major contributor to pathology (4, 5). Here, IFNA1 is linked to systemic lupus erythematosus.