Whether neonatal exendin-4 acts similarly in the IUGR lamb as in the PR rat, by reversing epigenetic changes in the Pdx-1 promotor and improves adult β-cell mass and function to delay or prevent the subsequent loss of insulin secretory capacity observed after IUGR in young adult male sheep [11] remains to be determined, and will require separate animal cohorts with long-term follow-up of functional and molecular outcomes. The gene discussed is INS; the disease is fetal growth restriction.