Overall, our observations in this study support a possible dual role of NK cells in the inflammatory process underlying the disease pathogenesis of SS: following an initial insult on the SGs, NK cells interact directly with apoptotic/damaged EC possibly through NKp30 and B7/H6, respectively, resulting in the production of pro-inflammatory cytokines/chemokines and influx of more effector cells. This evidence concerns the gene NCR3 and synovial sarcoma.