Of importance, here we showed that hyperactivated IFN-α/JAK1/STAT1 signaling, in concert with increased STING-dependent IFN-α production in Ncf1m1j/m1j pDCs, acting as a positive feedback loop, augments type I IFN responses, which may be crucial to lupus exacerbation driven by ROS deficiency. The gene discussed is STAT1; the disease is systemic lupus erythematosus.