CD25/IFN-γ DKO mice had delayed glandular destruction and preserved secretory function at 8 W [13], in agreement with findings in the NOD model of SS where deletion of IFN-γ improved sialodenitis, decreased caspase-3 activity and TUNEL+ cells compared to parental NOD strain [12]. This evidence concerns the gene CASP3 and synovial sarcoma.