Human red blood cells metabolically engineered with the recombinant enzymes guanidinoacetate methyltransferase (GAMT) and methionine adenosyl transferase (MAT) perform in vitro as competent bioreactors to reduce guanidinoacetate acid and produce creatine, thus representing a potential strategy to treat patients with GAMT deficiency and a platform for novel therapeutic approaches. The gene discussed is GAMT; the disease is hyperinsulinemic hypoglycemia, familial, 4.