The MMR system has evolved to increase the fidelity of DNA replication and homologous recombination 1 . MMR is also implicated in the processing of other types of DNA damage, as mammalian cells with defective MMR are tolerant to S N 1 type methylating agents such as N-methyl-N′-nitro-N-nitrosoguanidine and to 6-thioguanine and cisplatin 2 . Reports describing the differential sensitivity of MMR-proficient and -deficient cells to ionizing radiation raised some controversy, as MMR-deficient cells were found to be slightly more resistant to ionizing radiation in some laboratories 3 but either equally 4 or less resistant 5 in others. The survival differences were also questioned, because MMR status was reported to affect the length of the G2-M checkpoint rather than cell viability 6 . A report by Brown et al. 7 has reopened this discussion by describing the requirement of a functional MMR system for activating the S-phase checkpoint and signaling of ionizing radiation–induced damage. The aforementioned studies used matched MMR-proficient and -deficient mouse or human cell lines. Given that the establishment of these lines involved long periods of growth in cell culture, and that the MMR-deficient