TOR promotes cell growth, which is essential in early life. Later, however, it is unable to switch itself off even when the growth it drives becomes excessive, leading to cell deterioration and the onset of age-related diseases. They go on to suggest that while these pathways that cause aging cannot be completely switched off by a mutation (because that would be harmful or even lethal early in life), perhaps they can be inhibited by drugs such as rapamycin years later, when an uninhibited TOR becomes a problem after individuals have reached middle age.
