Cells are exposed to DNA damage, reactive oxygen species (ROS), high oncogenic signalling or to telomere shortening due to multiple replications. (2) If no repair or cell cycle arrest checkpoints are operative, cells might undergo immortalization and transformation as first steps of tumorigenesis or (3) cells might undergo cellular senescence or apoptosis. The senescent cells then (4) show an altered secretory phenotype and thus influence signalling, or (5a) they might be removed after undergoing senescence by apoptosis or by the immune system. This in turn (5b) leads to replication/transdifferentiation of neighbouring cells or of replication/differentiation of adult stem and progenitor cells, decreasing their proliferative potential. Finally, (6) the senescent cells display an altered behaviour and physiology in regard to their ‘daily’ tasks within a tissue. All this in turn leads to (7) changes in the microenvironment of tissues and to their functional decline, which in turn (8) enhances the risk of tumor development and (9) accelerates senescence, thus largely contributing to aging of organisms