The role of the mitochondria in the process of carcinogenesis has drawn researchers' attention since the discovery of respiratory deficit in cells, particularly those characterized by rapid proliferation. The deficit was assumed to stimulate further differentiation of the cells and initiate the process of neoplastic transformation. As many as 25-80% of somatic mutations in mitochondrial DNA (mtDNA) are found in various neoplasms. These mutations are considered to trigger the neoplastic transformation through shifts of cell energy resources, an increase in the mitochondrial oxidative stress and modulation of apoptosis. The question arises as to whether the mtDNA mutations precede a neoplasm or whether they are a result of changes and processes that take place during neoplastic proliferation.