When human breast cancer cells, defective in Complex I activity, are transfected to express yeast NADH dehydrogenase, Ndi1, their ability to oxidize mitochondrial NADH is restored and, at the same time, their tumor forming ability in xenografts is substantially reduced.79 Given that the Ndi1 expression enhances the NAD+/NADH ratio in whole cells and mitochondria, the effect was analyzed by supplying NAD+ precursors, NicA and NAM80 to the same Complex I-defective breast cancer cells. The gene discussed is ENSG00000251605; the disease is breast carcinoma.