Fig. 2. Choice of response to p53 may reflect differential regulation of cell cycle arrest, and apoptotic and survival promoters. Low or repairable levels of stress or damage result in the induction of cell cycle arrest, and repair and survival signals by p53. More severe, irreparable or oncogenic stress leads to the activation of apoptotic signals, possibly accompanied by a decrease in expression of the survival genes (Bensaad et al., 2006).