Additionally, in cultured primary microglia, we found that unlike lipopolysaccharide (LPS, a TLR agonist and classic microglia activator) and IFNα (a reported microglia activator in lupus mice), C1q did not alter the transcription of IFN-inducible genes or NF-κB-dependent proinflammatory cytokines at the tested doses (0–50 μg/mL C1q) (Supplementary Fig. 7c) and failed to change phagocytic activity compared to IFNα and LPS (Supplementary Fig. 7d, e). The gene discussed is NFKB1; the disease is systemic lupus erythematosus.