TK1 and cancer: In normal, transformed, and cancer-derived cell lines, Fhit-depletion causes replication stress-induced DNA double-strand breaks [7, 8] and defects in replication fork progression, through down-regulation of Thymidine Kinase 1 (TK1) expression and reduced thymidine triphosphate pool levels; thymidine supplementation rescues DNA replication defects and suppresses DNA breakage in Fhit-deficient cells.