Type 1 diabetes is the result of destruction of insulin producing beta cells by T cells. Our group has been studying the role of cytokines in orchestrating the events leading up to beta cell destruction. Interferon-g creates a proinflammatory environment in the pancreatic islets and facilitates recognition and killing of beta cells by CD8+ T cells through upregulation of MHC class I on beta cells. Activation, proliferation, and survival of beta cell specific T cells depend on cytokines that use the common g chain of the IL-2 receptor. JAK inhibitors, which block signalling downstream of cytokine receptors, have been developed for treatment of autoimmune and inflammatory disorders. Our preclinical data show that JAK inhibitors prevent and reverse autoimmune diabetes in the NOD mouse model of T1D. We conducted the BANDIT study to test the efficacy of the JAK inhibitor baricitinib in a phase 2 clinical trial in new-onset T1D. Results from the study will be presented.