Most research articles pertaining to type 1 diabetes (T1D) begin with prose such as, "T1D develops due to a T-cell mediated destruction of insulin producing pancreatic beta cells", "The onset of T1D occurs when 85 to 95% of beta cells have been destroyed", and "While the pathogenesis of T1D remains unclear, viral triggers are likely involved". These notions have, over the yeas, to some extent, developed into 'dogmas'.1 However, the reality is one where major shortcomings in knowledge with respect to disease pathogenesis exist. T1D is a difficult disorder to investigate given: variances in the age at symptomatic onset; a long prodromal state of pre-diabetes; an inability to effectively examine the target organ (i.e., the pancreas); its polygenic nature; and more. As a result, most investigations to date have examined indirect features or models of the disease (e.g., animals, peripheral blood, in vitro analysis of surrogate beta cell lines). Therefore, in 2007, the JDRF Network for Pancreatic Organ donors with Diabetes (nPOD) was formed.2 NPOD has pioneered means for recovering pancreata from donors with T1D & non-diabetic donors with T1D-associated autoantibodies and providing them to investigators worldwide. Since inception, nPOD has recovered over 225 cases including 110 with different forms of diabetes and 19 non-diabetic donors with T1D-associated autoantibodies (note: 15 cases with insulitis). Exciting findings are emerging: T cells reactive to islet autoantigens have been identified in pancreatic islet infiltrates; insulitis and insulin-positive pancreatic beta cells persist many years after diagnosis; pancreatic size is reduced in T1D; pathogeneic mechanisms beyond T cell-mediated autoimmunity have been suggested; and more. nPOD is also implementing a research model based on real-time data sharing and joint analyses of common samples. This presentation will share this information and describe nPOD's ultimate purpose to accelerate the pace of discovery and identify a cure for T1D.