It is tempting to speculate that the enrichment for NOTCH gene signatures implies altered NF-κB-Relb signaling in CD1c+ DCs, with a mechanism that varies between diseases mediated by type I IFNs (e.g., SLE) and type I IFN-negative diseases (e.g., uveitis). The gene discussed is NFKB1; the disease is systemic lupus erythematosus.