A full account of the physiology behind this discordance is outside the scope of this review, but may include (a) more synchronous T cell infiltration into pancreatic islets in NOD mice than in at-risk human subjects, (b) the potential for a greater dependence on CD8 T cells in diabetes pathogenesis in human disease (10), and (c) confounding effects of multiple concurrent T cell responses in human patients exposed to the “universe” of viral and bacterial pathogens as opposed to inbred specific pathogen-free NOD mouse colonies. This evidence concerns the gene CD8A and diabetes mellitus.