It can thus be assumed that the phenotypic effects observed in Aaas KO/Sod2 Het mice in the present study are caused by both the Warburg effect and increased expression of Nnt. These additive actions lead to transient increase of glutathione oxidative capacity and to an enhancement of the compensatory effect seen in Aaas KO mice, which lack typical symptoms of triple A syndrome. The gene discussed is AAAS; the disease is Triple A syndrome.