Reactive oxygen species are important in carcinogenesis, diseases, and aging, probably through oxidative damage of DNA. Our understanding of this relationship at the molecular level is very sketchy. It has recently been found that in mitochondria oxidative DNA damage is particularly high and may not be repaired efficiently. I propose that oxidatively generated DNA fragments escape from mitochondria and become integrated into the nuclear genome. This may transform cells to a cancerous state. Time-dependent nuclear accumulation of mitochondrial DNA fragments may progressively change the nuclear information content and thereby cause aging. This proposal can be tested experimentally.