The human studies that demonstrated decreased 24-hour recoveries of transfused RBCs from G6PD-deficient donors used autologous transfusions of radiolabeled RBCs; as such, the G6PD-deficient RBCs were not only exposed to the oxidative stress of storage but also introduced into a recipient with potentially altered redox biology due to G6PD deficiency. The gene discussed is G6PD; the disease is hyperinsulinemic hypoglycemia, familial, 4.