That NER could be the pathway inhibited by aphidicolin in CLL cells in response to purine analogs is supported by several observations: (1) the repair of UV-C-induced DNA damage, known to occur by NER, was inhibited by aphidicolin, (2) XPA, an essential factor for NER, was translocated from the cytosol to the nucleus after fludarabine, as previously observed after UV and alkylating agent treatment [28, 29, 38], and (3) silencing of XPA in cell lines, including a CLL cell line, resulted in higher caspase-3 activation in response to fludarabine. Here, XPA is linked to B-cell chronic lymphocytic leukemia.