FasL, perforin, $TNF{alpha}$, IL-1 and NO have been considered as effector molecule(s) leading to ${eta}$-cell death in autoimmune diabetes. However, the real culprit(s) of ${eta}$-cell destruction have long been elusive despite intense investigation. Previously we have suggested $IFN{gamma}/TNF{alpha}$ synergism as the final effector molecules in autoimmune diabetes of NOD mice. A combination of $IFN{gamma}$ and $TNF{alpha}$ but neither cytokine alone, induced classical caspase-dependent apoptosis in murine insulinoma and pancreatic islet cells. $IFN{gamma}$ treatment conferred susceptibility to $TNF{alpha}$-induced apoptosis on otherwise resistant murine insulinoma cells by STAT1 activation followed by IRF-1 induction. Here we report that $IFN{gamma}/TNF{alpha}$ synergism induces apoptosis of human pancreatic islet cells. We also observed STAT1 activation followed by IRF-1 induction by $IFN{gamma}$ treatment in human islet cells. Taken together, we suggest that $IFN{gamma}/TNF{alpha}$ synergism could be involved in human islet cell death in type 1 diabetes, similar to murine type 1 diabetes.