Cellular senescence, a process that limits the proliferation of normal human cells, has been linked to both tumor suppression and aging. Recent studies have revealed that cellular senescence also promotes tissue repair and fuel inflammation associated with aging and cancer progression. This complex process involves four main biological processes: tumor suppression, tumor promotion, aging, and tissue repair. The challenge is to understand the senescence response well enough to harness its benefits while suppressing its drawbacks. Cellular senescence is initiated by various stimuli, including oncogenic stress, telomere erosion, and DNA damage. Senescent cells exhibit several phenotypes, such as an irreversible growth arrest, expression of SA-Bgal and p16INK4a, secretion of growth factors and cytokines, and nuclear foci containing DDR proteins. Senescence is crucial for tumor suppression, as it prevents the growth of cells at risk for neoplastic transformation. However, senescent cells can also promote cancer progression through cell nonautonomous mechanisms. Additionally, senescent cells contribute to aging and age-related diseases, possibly by depleting stem or progenitor cells, disrupting tissue structure and function, and promoting chronic inflammation. The senescence response may also play a role in tissue repair, as it helps resolve normal tissue damage. The temporal organization of the senescent phenotype involves a decision period, the expression of SASP proteins, immune clearance, and negative feedback loops. Understanding the complex regulation of cellular senescence will help in developing strategies to harness its benefits and mitigate its drawbacks.Cellular senescence, a process that limits the proliferation of normal human cells, has been linked to both tumor suppression and aging. Recent studies have revealed that cellular senescence also promotes tissue repair and fuel inflammation associated with aging and cancer progression. This complex process involves four main biological processes: tumor suppression, tumor promotion, aging, and tissue repair. The challenge is to understand the senescence response well enough to harness its benefits while suppressing its drawbacks. Cellular senescence is initiated by various stimuli, including oncogenic stress, telomere erosion, and DNA damage. Senescent cells exhibit several phenotypes, such as an irreversible growth arrest, expression of SA-Bgal and p16INK4a, secretion of growth factors and cytokines, and nuclear foci containing DDR proteins. Senescence is crucial for tumor suppression, as it prevents the growth of cells at risk for neoplastic transformation. However, senescent cells can also promote cancer progression through cell nonautonomous mechanisms. Additionally, senescent cells contribute to aging and age-related diseases, possibly by depleting stem or progenitor cells, disrupting tissue structure and function, and promoting chronic inflammation. The senescence response may also play a role in tissue repair, as it helps resolve normal tissue damage. The temporal organization of the senescent phenotype involves a decision period, the expression of SASP proteins, immune clearance, and negative feedback loops. Understanding the complex regulation of cellular senescence will help in developing strategies to harness its benefits and mitigate its drawbacks.