The T cell mediated autoimmune origin of T1D has prompted efforts to prevent disease progression by targeting T lymphocytes using immunosuppressive drugs including cyclosporine,1 anti-CD3 antibody treatment,2 antithymocyte globulin3 and anti-CD80 and anti-CD86 antibody treatment.4 5 However, these treatment strategies have (at best) a temporary impact on disease progression with no effect on long-term progression and are accompanied by serious side effects.6 7 Therefore, additional insights into T1D pathophysiology are urgently needed to find novel therapeutic interventions. The gene discussed is CD86; the disease is type 1 diabetes mellitus.