Chow et al may explain the lack of correlation mentioned before and account in part for the synergistic affect of both drugs reported by our group. Nevertheless, the fact that we did not find a correlation between the CLB IC 50 in the presence of STI571 and the STI571 IC 50 is not in keeping with this hypothesis. Moreover, it has been shown that in CHO cells, proteolytic inactivation of Rad51 by a caspase-mediated mechanism contributes to the cell death response induced by IR-mediated DNA damage. 4 If this mechanism takes place in human B-lymphocytes, STI571 may decrease Rad51 related homologous recombinational repair (HRR) not only by decreasing c-abl-mediated Rad51 phosphorylation 5-7 and consequently HRR but also decreasing Rad51 protein levels. We summarize the possible pathways involved in STI571 and CLB-induced apoptosis in B-lymphocytes in Figure 1.