The tumor-promoting effects of mitochondrial genome mutation, such as in the genes encoding subunit 1 of cytochrome oxidase (CO) or various subunits of NADH dehydrogenase (ND) is due in part to increased levels of cytosolic and mitochondrial reactive oxygen species (ROS) resulting from electron escape from the respiratory chain when these genes products have reduced function (19–21, 23, 24). This evidence concerns the gene AQP1 and neoplasm.