34 The War on Aging they make these structures less elastic and thus more prone to mechanical damage. The most promising first-generation therapy to eliminate such cross-links is a molecule known as ALT-711. [15] However, it breaks only one class of such link, known as dicarbonyl bonds. [16] Numerous other classes have been  identified.  [17]  Worse,  many  are  thermodynamically much more stable than dicarbonyl bonds, giving reason to doubt that non-toxic small molecules could ever cleave them. More elaborate approaches (already under consideration, but beyond the scope of this article) may thus be needed in order to limit the abundance of crosslinks indefinitely. THE ‘ESCAPE VELOCITY’ TRANSITION The above considerations constitute an acknowledgement that aging will never be cured in the sense that a bacterial infection  is  cured,  i.e.  entirely  eliminated  from  the  body. Rather, it will be cured in the sense that malaria or AIDS can presently be cured: it can be controlled very well given access to appropriate medication whenever needed, but that medication can never be confidently dispensed with forever. It may not be clear to the reader, however, that what I have said above allows even that degree of ‘cure’ of aging. The  reason  it  does  so  can  be  summed  up  in  one  word: bootstrapping. The second-generation therapies will not be needed for at least two decades after the first-generation thera- pies arrive, because that is how long it will take before the “seven deadly things” return to the life-threatening level that they attained before those therapies arrived. Thus, so long as the second-generation therapies do indeed arrive within two decades, we will be broadly in the same position as regards mortality rates, as if they had arrived at the same time as the first-generation. The same logic clearly extends to subsequent