Apoptosis, or programmed cell death, ensures that injured cells do not replicate and pass on genomic DNA damage to progeny cells. Therefore, the inability to proceed with apoptosis after severe damage is disadvantageous for an organism, since replication of lesion-containing DNA can lead to the immortalization of genomic mutations and, potentially, to tumor formation (62). Indeed, many tumors exhibit defects in proteins important in apoptosis; the p53 protein is a good example, since it functions in promoting apoptosis after stress and is one of the most frequently mutated genes in human tumors (63). On the other hand, the cell must also have proteins that negatively regulate apoptotic pathways in the event that stress-induced damage is efficiently repaired, and Wip1 is one of these proteins (Figure 4).
