A striking feature of Fanconi anemia (FA) cells is their hypersensitivity towards crosslinking agents such as mitomycin C (MMC). In this study, we have shown that treatment of lymphoblastoid cells with MMC resulted in nuclear fragmentation, chromatin condensation, and DNA degradation, which is characteristic of apoptosis. The level of DNA fragmentation 48 hours after MMC treatment reached approximately 33% in both control and FA cells. In addition, 24 hours after drug addition a decrease in the number of cells in the G2/M phase of the cell cycle was seen. This coincided with the appearance of apoptotic cells in the sub-G1 phase, indicating that once the cells had passed through G2/M, apoptosis occurred. The number of apoptotic cells increased to 60% 96 hours after MMC treatment. The number of apoptotic cells increased to 60% 96 hours after MMC treatment. The onset and level of apoptosis was found to be identical in FA and control cell lines, indicating that the FA defect does not lead to abnormal apoptotic cell death.