This interesting research result adds a little more to the debate over whether nuclear DNA damage is relevant to aging beyond its effects on cancer risk - though I think it's still a bit early to point to differences in DNA repair as the definitive cause of SIRT6-related longevity in mice: researchers "found that the decline in a cell's ability to repair DNA during aging coincided with a global reduction in the levels of proteins involved in the repair process. [They] tried to reverse the age-related decline in DNA repair efficiency by restoring the proteins to their original levels and found only one protein, SIRT6, did the trick. ... [Other research results have shown] that overexpressing the SIRT6 protein extended the lifespans of mice. Our research looked at DNA repair and found a reason for the increased longevity, and that is SIRT6's role in promoting more efficient DNA repair. ... The next step [is] to study the factors that regulate SIRT6, in an effort to learn more about the early stages of the DNA repair process. ... multiple groups are trying to develop drugs that activate SIRT6, and [researchers hope] that this research will one day lead to therapies that help extend a person's lifespan and treat cancer. ... SIRT6 plays a critical role in repairing the most dangerous type of DNA damage: double-strand breaks. DNA is a two-stranded molecule, and breaks can occur to one strand of the molecule or to both. In the case of single-strand breaks, the unbroken strand guides the repair process and the DNA molecule is typically restored to its original state. However, double-strand breaks, in which both strands are severed, are particularly hazardous because they are more difficult to repair and can lead to a rearrangement of the cell's genetic material."