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Type 1 diabetes results from autoimmune damage to βcells and insulitis typically characterizes its pathological presentation. Apoptosis could be a main mechanism.There are several pathways of apoptosis including FasFasL. 1 Fas is a type 1 transmembrane glycoprotein in the super family of TNF/NGF receptors and FasL (the specific ligand for Fas in vivo) is a type 2 transmembrane glycoprotein in the super family of TNF. 2 Their interaction for inducing apoptosis is important in many processes. 3 Their malfunction can lead to the overproliferation of the autoreactive immune cells in mice or humans. 4-5 In autoimmune diabetes, specific CDs + T cells may kill β cells by FasL and perforin-granuzyme.Moreover, Fas-FasL also mediates the elimination of autoreactive T cells. 6-11 Diabetes in nonobese diabetic (NOD) mice is a result of autoimmune damage to βcells. 12 Our study aims at analyzing the significance of Fas-FasL in NOD insulitis, specifically discussing the mechanism of autoimmune diabetes.