With nucleic acid stimulation, patient-derived monocytes produced significantly higher IFN-α and IL-6 levels in response to poly(dA:dT), poly(I:C), and CL097 stimulation (Figure 5F and Supplemental Figure 2, E and F) These results implied that patient-derived monocytes are more susceptible to producing IFN-I and inflammatory cytokines under exposure to nucleic acids originating from cell debris, ICs, and pathogen infections, which further promote the development of the IFN-I signature and inflammation in SLE patients. The gene discussed is IFNA2; the disease is infection.