For example, IFN-α overexposure might explain the lack of functional CD24+CD38hi Breg cells, and bias toward anti-nuclear antibody production and more severe disease, in patients with SLE who have an “IFN gene signature.” In MS patients, IFN-β treatment can induce the development of thyroid autoimmunity (Frisullo et al., 2014) and failure to respond to treatment in patients with an existing “IFN gene signature” (Verweij and Vosslamber, 2013). This evidence concerns the gene IFNA1 and systemic lupus erythematosus.