TP53 and neoplasm: Although this senescence response has been shown to involve many of the same DNA damage response mediators (e.g., ATM, ATR, Chk1, Chk2) as those activated by telomere dysfunction and oncogene activation, it is noteworthy therapeutically that cancer cells lacking functional tumor suppressors such as p53 or pRB often retain the capacity to undergo external agent-induced senescence.