Studies in insulinoma cells have shown that glucose-stimulated insulin release is enhanced upon peroxiredoxin 3 knockdown and blocked upon peroxiredoxin 3 overexpression170, and peroxiredoxin 3 knockouts have elevated fasting insulin plasma levels and are insulin resistant171, suggesting a potentially conserved function for prdx-3 and mammalian peroxiredoxin 3 in inhibiting DCV secretion by the removal of mtH2O2. This evidence concerns the gene INS and pancreatic insulinoma.