Reprogramming of acinar cells toward functional β-like cells would offer an abundant and autologous source of insulin-producing cells. The current literature suggeststhat manipulation of genetic factors,in combination with cytokines or small molecules targeting specific pathways and the epigenetic machinery in humans,may eventually yield functional acinar-derived β-like cells. Our preliminary datashowthat treatment of adult mice with a compound that specifically inhibits the kinase activity of focal adhesion kinase (FAK) results in transdifferentiation of acinar cells into insulin-producing cells. Notably, the acinar-derived insulin producingcells infiltrate the pre-existing endocrine islets and are able to normalize the blood glucose levels.Here, we seek to determine whether FAK inhibition would convert human acinar cells into insulin-producing cells.