HEREDITARY methaemoglobinaemia, a rare disorder often associated with a deficiency in NADH-dependent ‘diaphorase’ activity1, has been treated successfully with methylene blue (1–2 mg/kg intravenously) or ascorbic acid (200–500 mg/day orally)2. Methylene blue probably effects the reduction of methaemoglobin by activating the NADPH-dependent methaemoglobin reductase that has been isolated, from human erythrocytes by Kiese et al.3 and by Huennekens et al.4. By serving as electron carriers between NADPH and the methaemoglobin reductase, methylene blue and other artificial electron carriers increase the activity of the hexose monophosphate shunt pathway of glucose metabolism5 and facilitate the reduction of methaemoglobin to haemoglobin. This NADPH-dependent methaemoglobin reductase system is a reserve mechanism for the reduction of methaemoglobin, for the NADH-dependent ‘diaphorase’ system appears to be the physiologically important pathway in normal human erythrocytes. Ascorbic acid can reduce methaemoglobin to haemoglobin slowly both in vivo and in vitro, probably through a direct effect on the methaemoglobin2.