Notably, despite the use of ATR inhibition as a monotherapy strategy to target chronic lymphocytic leukemia cells with TP53 defects [43], our results showed that breast cancer cells with high expression of RNF126 had enough endogenous replication stress via CDK2 to mediate and affect the sensitivity to ATR inhibitors in breast cancer cells with or without wild-type TP53 (Fig. 5P). This evidence concerns the gene RNF126 and B-cell chronic lymphocytic leukemia.