Given that the Akt pathway is critical for cell survival, and cancer cells have been suggested to demonstrate increased intracellular hydroperoxide production compared to normal (untransformed) cells [2, 9–11], we propose that tumor cells may increase Akt activity to compensate for increased intracellular hydroperoxides and oxidative stress caused by defects in mitochondrial respiration. This evidence concerns the gene AKT1 and neoplasm.