Our aim is to find out whether human exocrine cells have the same capacity for transdifferentiation which we previously demonstrated for rodent cells. Our hypothesis is that sufficiently high activation of STAT3 and MAPK intracellular pathways induces the transdifferentiation of exocrine acinar to endocrine beta cells. This will be tested with a genetic and a non-genetic approach. In addition, we will examine the role of Notch-signaling. If human acinar cells can be reprogrammed into functional beta cells, this could mean an important advancement in the field of cell therapy for diabetes.