Early in the process of embryonic development all sorts of radical restoration of damage takes place, things that couldn&#x27;t happen in an adult organism without severe disruption. Telomere lengthening via telomerase is just one of them. E.g.:<p><a href="http:&#x2F;&#x2F;phys.org&#x2F;news&#x2F;2011-09-body.html" rel="nofollow">http:&#x2F;&#x2F;phys.org&#x2F;news&#x2F;2011-09-body.html</a><p>Early embyros have a lot in common with negligibly senescent lower species like hydra in that they are in a state of always-on regeneration. Repair everything, all the time. That state of being was lost somewhere along the way to organisms that have complex nervous systems made up of long-lived cells and structures that have to record state. An adult human couldn&#x27;t operate like a hydra and live.<p>The setup for most species is that adults have small groups of stem cells with telomerase and unlimited self-renewal, but the bulk of tissue is made up of somatic cells without telomerase, or with much less telomerase activity, that have a limited number of divisions before self-destruction or clearance by the immune system. Stem cells produce in a small number of new somatic cells as needed, and are the only tiny set of cells with the unlimited replication privilege. Telomere length is a part of the countdown mechanism that limits divisions in somatic cells - see the Hayflick Limit - because of the end replication problem in that a little of the length is lost with each cell division. This situation is shaped by the existence of cancer. The whole arrangement looks very much like something that came into being to fend off cancer, with ever more checks and balances arising to prevent uncontrolled replication, while still incorporating the mechanisms needed for embryonic growth and later regeneration.