The repair of mitomycin C (MMC)-induced DNA crosslinking was analyzed by denaturation-renaturation gel electrophoresis in ribosomal RNA genes in lymphoblastoid cell lines from 4 patients with Fanconi's anemia (FA). In comparison to normal lymphoblastoid cell lines, 2 lines of FA cells belonging to complementation group A clearly exhibited higher sensitivity to MMC and an almost identical deficiency in the removal of DNA crosslinking. A complementation group B cell line, HSC 62, exhibited a lower sensitivity than group A cells and a lesser deficiency in crosslink repair. Another 'non-A' group cell line, HSC 230, reproducibly exhibited even higher sensitivity to MMC than group A cells. The results on MMC crosslinkage removal at the molecular level correlated well with cell survival. The observed subtle differences of repair among the 4 FA cell lines might represent possible genetic differences in the respective FA complementation groups.