Beta-cell death, and the consequent deficiency in insulin secretion, is a key feature of type 1 diabetes. For decades, the standard of care for this disease has been insulin therapy by intramuscular injection. Current approaches to develop new treatments have prioritized islet transplantation and directed stem-cell differentiation, while many technological advances have focused on glucose detection and insulin delivery. While cell-based treatments show promise, a chemical intervention capable of restoring glycemic control in type 1 diabetes would have enormous impact clinically, by enabling an in vivo pancreatic effect while avoiding the need for immunosuppression. Bridget’s group is developing phenotypic-cell based assays to find compounds that increase human beta-cell proliferation, that can protect beta cells from the inflammatory processes of diabetes progression, or that can induce beta-cell transdifferentiation, in which other cells in the pancreas take over the role of beta cells by producing insulin themselves.