Although these observations in CD8+ T cells were restricted to the initiation phase of autoimmune T1D when the PLN was crucial for the development of diabetes (~10w)39, these results suggest that the defective proliferation and/or reduced number of CD8+ CTLs, which are the primary effector immune cells for β-cell destruction38, in the PLN are responsible for the inhibition of autoimmune T1D development in Tyk2−/− NOD mice. The gene discussed is CD8A; the disease is diabetes mellitus.