Given that both PD and POLG neurons show a similar pattern of multiple mtDNA deletions2, mtDNA copy number was found to be higher in PD neurons than those with POLG mutations4, explaining the potential of PD neurons to compensate for a certain degree of mitochondrial deficiency via an increase in mitochondrial mass. Here, POLG is linked to hyperinsulinemic hypoglycemia, familial, 4.