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. The gene discussed is AKT1; the disease is cancer.