“…Conditions that trigger senescence include genomic instability, extreme telomere shortening, metabolic and proteostatic stress, reactive oxidative species (ROS), oncogene activation, mitochondrial dysfunction, epigenetic changes, and other mechanisms that have not been fully clarified (Childs, Durik, Baker, & van Deursen, ; Childs et al, ; López‐Otín et al, ). In general, these conditions trigger a response that activates the tumor suppressor genes p53, p16 Ink4a , and p21 that utilize different pathways to induce cell cycle arrest (Hall et al, ; Liu et al, ). Most studies indicate that senescence‐induced replication arrest acts as a tumor suppression mechanism, but other physiological roles are emerging, including fetal organ development, wound healing, and aging (Baker & Petersen, ; Pratsinis, Mavrogonatou, & Kletsas, ; Wiley & Campisi, ; Zhang, Chen, Liu, Chen, & Liu, ).…”