RAB3A and Glucose intolerance: Genetic models support this view, as deletion of the Rab3A [25], or Rab27a [26] G protein in mice results in hyperglycemia, hypoinsulinemia and glucose intolerance, whereas transgenic expression of a dominant negative Rac1 mutant in β cells impairs islet morphogenesis, potentially by interfering with migration of pancreatic β cells away from the ductal epithelium [27].