As IFNs have been shown to induce the transcription of STAT1 in monocytes48 and increased transcription could lead to an increase in unphosphorylated STAT1 and a prolonged IGS in the absence of IFNs49 transcripts for STAT1 were evaluated and shown to be elevated in both active and inactive SLE WB, PBMC, and monocyte datasets, but not in T and B cells from inactive SLE patients (Fig. 9g). The gene discussed is STAT1; the disease is systemic lupus erythematosus.