This study was initiated to investigate a possible strategy to alter an enzyme deficiency in a mouse model. The enzyme investigated is a multifunctional nucleoside kinase from Drosophila melanogaster (Dm-dNK). This enzyme has special features in that it has higher enzymatic activity than any other known nucleoside kinases and still has similar substrate specificity as the human nucleoside kinases. The deficiency where the Dm-dNK transgenic mice model will be used is a TK2 deficient model with severe phenotype caused by mitochondrial DNA depletion. The Dm-dNK transgenic mice model will be used as a way to rescue the TK2 deficient mice.