Dermatomyositis (DM) frequently remains active despite glucocorticoids and conventional immunosuppressants. A type I interferon (IFN-I) gene-expression signature across skin, muscle, and blood provides a biologic rationale for IFNAR1 blockade [1–3]. Anifrolumab, an anti-IFNAR1 monoclonal antibody, is effective and steroid-sparing in systemic lupus erythematosus [4].
