Recent genome-wide association studies (GWAS) have shown a strong correlation between a genetic polymorphism in the SH2B3gene and the development of autoimmune diseases, including type 1 diabetes (T1D). Lnk/Sh2b3 is an adaptor protein interacting with various intracellular proteins involved in JAK/STAT cytokine signaling of different cell types, including CD8 T cells. Additionally, Sh2b3-deficient CD8 T cells are hypersensitive to IL-15 stimulation. However, how reduced Sh2b3 function affects the molecular mechanisms that activate and sustain CD8 T cells promoting T1D development remains elusive. We hypothesized that genetic deletion of Sh2b3 in the non-obese diabetic (NOD) mouse would impact T1D incidence by altering T cell activation. NOD. Sh2b3−/− mice developed diabetes faster than wild-type controls. Additionally, Sh2b3-deficient CD8 T cells were hyperresponsive to IL-15 stimulation, promoting the generation of the activated CD44 high CD8 T cell population. Intriguingly, IL-15-stimulated Sh2b3−/− splenocytes possessed significantly higher mitochondrial respiratory capacity (SRC) and ATP synthesis than the wild-type counterparts. Furthermore, CD8 T cells of NOD. Sh2b3−/− mice showed increased expression of genes associated with mitochondrial biogenesis and oxidative metabolisms in response to in vitroIL-15 stimulation. Overall, our study supports a role of Sh2b3 in T1D development by regulating mitochondrial biogenesis and metabolism of IL-15-stimulated CD8 T cell. Our study provides new insight into the role of Sh2b3 in activating and sustaining the CD8 T cell response in the pathogenesis of T1D.