The enhanced ABC formation was controlled by IL-21 and IRF5: the lack of SWEF, seems to lead to IRF5 dysregulation in response to stimulation with IL-21.32 Of note, DEF-6 serves as a genetic risk variant for human SLE,33 further supporting the notion that SWEF are also relevant to human SLE. The gene discussed is IRF5; the disease is systemic lupus erythematosus.