The following statement are true about tumor suppressor gene p53, except

Ref Robbins 7/e p302; 303; 8/e p290- 291,9/e p293-294 TP53 Gene: Guardian of the Genome The p53-encoding tumor suppressor gene, TP53, is one of the most commonly mutated genes in human cancers. The p53 protein thwas neoplastic transformation by three interlocking mechanisms: activation of temporary cell cycle arrest (termed quiescence), induction of permanent cell cycle arrest (termed senescence), or triggering of pro- grammed cell death (termed apoptosis). If Rb "senses" external signals, p53 can be viewed as a central monitor of internal stress, directing the stressed cells toward one of these three pathways. A variety of stresses trigger the p53 response pathways, including anoxia, inappropriate oncoprotein activity (e.g., MYC or RAS), and damage to the integrity of DNA. By managing the DNA damage response, p53 plays a central role in maintaining the integrity of the genome, as described next. p53-mediated cell cycle arrest may be considered the primor- dial response to DNA damage (Fig. 5-23). It occurs late in the G1 phase and is caused mainly by p53-dependent transcription of the CDKI gene CDKN1A (p21). The p21 protein, as described earlier, inhibits cyclin-CDK com- plexes and prevents phosphorylation of Rb, thereby arresting cells in the G1 phase. Such a pause in cell cycling is welcome, because it gives the cells "breathing time" to repair DNA damage.