Given that (in the absence of u-PA or plasminogen) systemic immune complex-mediated arthritis models are resistant to full disease development [3-5], it could be that synovial u-PA/plasmin is a critical component of an immune complex-mediated inflammatory reaction, perhaps indirectly by activating complement (C5a) [4], leading to cellular infiltration (as suggested previously [4,5,21]), rather than being involved directly in cell migration or tissue damage. The gene discussed is PLAU; the disease is arthritic joint disease.