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Human life expectancy has increased dramatically over the past two centuries, marking a significant public health achievement. While some projections predict a future where median lifespans reach 100 years, others contend that further longevity will depend on breakthroughs targeting the biological processes of aging. Recent studies in mice have demonstrated that telomerase activation, achieved via gene therapy and transgenic approaches, can extend both median and maximum lifespans substantially without an accompanying increase in cancer risk. We analysed survival data from three such studies using the Gompertz mortality model and show that these interventions reduce the slope parameter, indicative of a slower aging rate, rather than merely lowering baseline mortality. This observation challenges traditional models that assume independent, additive damage accumulation, suggesting instead that aging is driven by a limited number of interdependent processes with significant cross-talk. Mathematical modelling indicates that only three to five processes with substantial cross-talk may account for the observed deceleration. Extrapolation using Swedish survivorship data further implies that a reduction in the aging rate, similar to that seen in mice, could elevate the median human lifespan from 85 to over 100 years. These findings provide a compelling framework for developing targeted anti-aging interventions and a new perspective on the modifiability of the aging process.