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While it is generally accepted that T cells are critical for the development of diabetes in the non‐obese diabetic (NOD) mouse, the precise functions of the CD4⁺ and CD8⁺ subsets remain ill‐defined. Transfer experiments have provided evidence that CD4⁺ cells are the disease initiators, provoking massive mononuclear leukocyte infiltration into the pancreatic islets, while CD8⁺ cells play an effector role, responsible for the final destruction of islet beta cells. It was surprising, then, to find that NOD mice carrying a null mutation at the β2‐microglobulin (β2‐μ) locus, and thereby lacking major histocompatibility complex class I molecules and CD8⁺ T cells, developed neither insulitis nor diabetes. Here, we argue that the absence of insulitis in these animals results from their lack of CD8⁺ cells because islet infiltration is also absent when NOD mice are treated with an anti‐CD8 monoclonal antibody (mAb) at a young age …