ATR and neoplasm: PARP-inhibitor resistance has been associated with an increase in ATR-CHK1 pathway activity, due to PARP1 trapping, which results in the phosphorylation of several proteins that aid replication fork stability and facilitates the progression of DNA synthesis in PARP-inhibitor resistant tumor cells by overriding cell-cycle checkpoint signaling [77,79,81], thus increasing the sensitivity to ATR inhibitors [82].