It highlights disease-specific pathogenic mechanisms: promotion of osteoclastogenesis and chronic synovial inflammation via Granulocyte-macrophage colony stimulating factor (GM-CSF) and the IL-23/IL-17 axis in RA; amplification of type I interferon responses and autoantibody production in SLE; potential contribution to fibrosis through TGF-β secretion in SSc; and mediation of glandular injury through cytotoxicity in pSS. The gene discussed is CSF2; the disease is systemic lupus erythematosus.