Perhaps ironically, lengthening telomeres such as via telomerase therapies is one of the things that a lot of other researchers are hot on and is not actually on the SENS agenda.<p>Since those other researchers are definitely advocating progress towards the use of telomerase therapies in humans, and it is inarguably the case that telomerase gene therapy extends life modestly in mice, probably by stimulating stem cell activity, your point still seems incoherent. See for example this position piece by Maria Blasco: <a href="http:&#x2F;&#x2F;dx.doi.org&#x2F;10.12688&#x2F;f1000research.7020.1" rel="nofollow">http:&#x2F;&#x2F;dx.doi.org&#x2F;10.12688&#x2F;f1000research.7020.1</a><p>From my position telomere length looks a lot a measure of aging rather than a cause, and telomerase therapies are something I&#x27;d consider risky at this point in humans - our telomere dynamics and telomerase setup is very different from that of mice, and I don&#x27;t think it is safe to assume that slowing of aging and induced regeneration in mice without cancer risk is necessarily going to happen in humans. You don&#x27;t know until you try, of course, and there is a contingent that will be trying. Note that at least one human has already disagreed with that assessment and had telomerase gene therapy, the CEO of BioViva.<p>From the SENS perspective, telomere length is something that will take care of itself if you create rejuvenation by repairing the causes of aging. Average telomere length in tissues is a product of stem cell activity and cell turnover rate, and aging diminishes the former, and that is a reaction to rising levels of damage. Get rid of the damage and stem cells should get back to work because the signaling environment will revert back to how it is in youth.