Therefore, weakening the RSR by interfering with the ATR/CHK1 signaling axis seems to be a suitable strategy not only to prevent tumor formation in experimental models, supporting an essential role of ATR and CHK1, but also for killing established tumors displaying a high proliferative index, such as Eμ-MYC lymphoma, Burkitt lymphoma or AML30–33. This evidence concerns the gene CHEK1 and lymphoma.