Whilst the pathophysiology of SLE remains incompletely defined, a pivotal role for the type 1 interferon (IFN) family has emerged, as evidenced by the overexpression of interferon-stimulated genes (ISG) in 60-80% of SLE patients (3, 4), and more recently by the success of an IFN receptor (IFNAR) blocking agent in improving clinical disease activity in clinical trials (5). This evidence concerns the gene STING1 and systemic lupus erythematosus.