Together with the findings of Zheng and colleagues, who demonstrate that the C1Q-high inflammatory monocyte phenotype present in patients with Behḉet’s disease is in vitro inducible with IFNγ (44), this highlights the potential interactions of complement activation and IFN signaling in driving pathogenesis in the SJIA clinical spectrum, and the conserved role of this monocytic program across the pan-immune landscape. The gene discussed is IFNA1; the disease is Behcet disease.