As such, SLE patients were recognized to have a distinct gene expression signature characterized by the upregulation of a number of interferon stimulated genes (ISGs) (1, 2), and an accumulation of IFNα-producing pDCs at sites of inflammation such as renal tissue in patients with active lupus nephritis (3, 4). The gene discussed is STING1; the disease is systemic lupus erythematosus.