In a trial enrolling 231 SLE patients, treatment with the humanized anti-IFN-α IgG1 monoclonal Ab rontalizumab failed to meet the primary endpoint for reducing disease activity measured with the British Isles Lupus Disease Activity Group (BILAG)-2004 (primary endpoint) and SRI (secondary endpoint) at week 24 in all patients and in a subgroup of patients with high expression scores of IFN-regulated genes (interferon signature metric, ISM). Here, IFNA2 is linked to systemic lupus erythematosus.