During aging, cells accumulate random damage. A fundamental question in aging is how such a stochastic process may eventually lead to aging phenotypes. We tackle aging research through an integrative approach, combining physics-inspired theoretical frameworks, experimental validation, large-scale medical datasets, and comprehensive synthesis of the vast body of published research across diverse organisms. Our aim: Unraveling transcriptional deregulation as a process of loss of function in aging tissues, for personalized diagnostics and therapeutics. We wish to identify 'ageing-susceptible' cells and genesidentify 'ageing-susceptible' cells and genes, reveal the mutations or epimutations that drives transcriptional deregulation in aging, as well as identify their functional consequences.