IDDM results from pancreatic beta cell destruction by islet-reactive T cells, a process that involves beta cell apoptosis. FasL-Fas pathway plays a major role in pancreatic beta cell death. Fas-associated death domain protein (FADD), the component of the tumor necrosis factor receptor type 1 (TNF-R1) and Fas signaling complexes, is involved in TNF-R1- and Fas-induced apoptosis. Inhibiting the function of FADD will lead to blocking downstream apoptosis signal, which protects pancreatic beta cells from destruction by FasL-Fas pathway. In this study we constructed eukaryotic expressing vector of fusional protein FADDdel-GFP named pFADDdeI-GFP. After pFADDdel-GFP was transfected into NIT, the expression of FADDdel-GFP in NIT was detected by fluorescence microscopy and the resistance of NIT transfected with pFADDdel-GFP to cytotoxicity mediated by special T cells was detected by FACS and MTT. The results showed that NIT modified by pFADDdel-GFP obviously resisted cytotoxicity mediated by special T cells. Therefore, it may be useful in the prevention or treatment of IDDM by intervening FasL-Fas pathway. Cellular & Molecular Immunology. 2004;1(5):383-386.