ATM and B-cell chronic lymphocytic leukemia: We previously observed that PARP activity was very high in a pilot cohort of CLL cases [13] and hypothesised that defects in DNA repair (e.g. loss of p53 or ATM function), response to oxidative stress or oncogene activation could lead to up-regulation of PARP1 and greater reliance on PARP activity for survival of CLL cells.