TP53 and cancer: These include: (i) reversible dormancy via premature senescence [87,88,89,90]; (ii) reversible dormancy reflecting drug-tolerant persister cells, both preexisting and therapy induced [91,92]; (iii) cancer cell survival subsequent to engagement of apoptosis and other regulated cell death pathways [22,91,93]; and (iv) heterogeneity of p53 protein expression, which “may represent p53 mutant patches indicative of clonal expansion, epigenetic modifications, and/or a number of other possibilities” [94].