However, Cheon et al. have recently demonstrated that increased expression of STAT1 and STAT2 as a result of constitutive low level IFN-β expression gives rise to a novel transcriptional complex composed of unphosphorylated STAT1 and STAT2 complexed to IRF9 (71), which drives a subset of anti-viral genes that overlap directly with the most highly expressed ISGs thus far identified in SLE patients. Here, IRF9 is linked to systemic lupus erythematosus.