Consistently, exposure of mice to AZD6738 significantly enhanced the percentage of tumor cells that stained positive for phosphorylated KAP1 and H2AX in CTR9-depleted tumors while treatment of control animals with AZD6738 did not induce a significant increase in KAP1 or H2AX phosphorylation (Fig. 4d, e). This evidence concerns the gene H2AX and neoplasm.