Novel molecular mechanisms regulating cell fate decisions of iPSC and adult derived pancreatic progenitors Diabetes mellitus is a metabolic disorder characterised by hyperglycaemia following a loss of insulin-producing beta cells in the pancreas. Unfortunately, the pancreas is a low turnover organ with limited regenerative capacity. Therefore, we focus upon identifying the molecular mechanisms by which other pancreatic cell types can be converted into beta-like cells in order to restore glycaemic control. To address this question, we combine 3D cell culture, scRNAseq technologies and computational modelling in order to understand the molecular regulation of cell fate changes. These results will elucidate the fundamental biology of iPSC and adult progenitors plasticity and provide clues for how to unlock the regenerative capacity of pancreas progenitors for future therapies for diabetes.