Fas receptor signaling is essential for the induction of pancreatic β cell death in autoimmune diabetes, upon being engaged by its ligand FasL (CD95L). We found that early overexpression of this proapoptotic receptor on pancreatic β cells delayed diabetes onset and reduced diabetes incidence in the NOD mice, and its late overexpression in β cells does not have any protective effect on the disease onset. We have further explored whether early Fas expression on β cells promotes the immunodeviation of the autorreactive CD4+T repertoire to the T regulatory phenotype, at the expense of the proinflammatory, diabetes-causing Th1-Th17 phenotypes. We did not find an increased frequency of CD4+Treg cells in the peripheral lymphoid organs or increased FoxP3 expression in islets from NOD mice overexpressing Fas early in life. Diabetes protection was improved by neutralizing the Th17 response in transgenic mice, which suggests that protection mediated by Fas overerexpression is not due to the abrogation of the Th17 response, at least not exclusively.