As the expression of B7.1 in pancreatic β cells has been shown to trigger the development of T1D in conventional mice (12) and accelerate diabetes in the NOD mouse (13), we introduced the human costimulatory molecule B7.1 (hB7.1) under the control of the rat insulin promoter in pancreatic β cells onto the YES background to enforce the development of spontaneous T1D. Here, INS is linked to type 1 diabetes mellitus.