Given that 1) FdUrd is approved for the treatment of colon cancer; and 2) there are limited therapeutic options for these tumors because tumors with defects in MMR are commonly considered to be unresponsive to 5-FU-based therapies, our finding that PARP inhibitors robustly sensitize MMR-deficient cells to FdUrd raises the possibility that therapies that combine FdUrd with a PARP inhibitor may have activity against these tumors. This evidence concerns the gene MRC1 and colonic neoplasm.