IFNB1 and systemic lupus erythematosus: 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).