TP53 and cancer: OIS is the result of oncogene mutations leading to replication pressure and telomere attrition77; however, in the case of telomerase activation, cells with mutated oncogenes will enter a state of unlimited proliferation, at which time, if appropriate external stimuli are applied to the cancer cells, such as radiotherapy, chemotherapy, and so on, the activity of telomerase decreases, and the cancer cells will reactivate the oncogenes, such as p53, p21, and so forth, and will enter a state of senescence.78, 79