A study using a murine model of SS indicated that soluble anti-FasL antibody, FLIM58 induced destructive autoimmune lesions with an elevation of serum antibodies against 120-kD α-fodrin [62], suggesting that (at least in that murine model of SS) the generation of sFasL had the potential to inhibit activation-induced cell death and the subsequent increase of CD4+T cells. The gene discussed is CD4; the disease is synovial sarcoma.