We also characterized the mechanism of CSC killing by CHK1+RAD51 and CHK1+MRE11 inhibitors, showing that it involves the induction of replication stress followed by progression of replication stressed CRC-SCs through the interphase and their premature entry into mitosis, ultimately leading to caspase-dependent mitotic catastrophe. The gene discussed is CHEK1; the disease is colorectal carcinoma.