Many if not all autoimmune diseases have undercurrents of systemic disease as evidenced by the involvement of additional organ systems, e.g. the lungs in RA, the CNS in SLE, Sjogren’s and sarcoidosis, etc. We speculate that LNs draining organs with articular or extra-articular disease, as in lung or glandular involvement in RA, produce IFN as a consequence of sensing signals such as dead cell debris, chromatin complexes, neutrophil nets or antigens as complement tagged or immunoglobulin complexes [69], [73]. The gene discussed is IFNA1; the disease is rheumatoid arthritis.