The observation that reduced early virus replication blunted CD8+ T cell priming and prevented the onset of diabetes in a model of virus-induced diabetes led to the discovery that early virus replication in dendritic cells is essential to disrupt immune tolerance and that this process is dependent on expression of ubiquitin specific peptidase 18 (USP18), an inhibitor of the IFNγ pathway [67]. This evidence concerns the gene CD8A and diabetes mellitus.