For instance, simultaneous treatment with AXL and ATR inhibitors induces replication fork collapse and double-strand breaks (DSBs), as indicated by increased levels of phospho-RPA32 and γH2Ax proteins, ultimately leading to mitotic catastrophe.172 In ovarian cancer cells, combining chemotherapy with a GAS6/AXL inhibitor (AVB-500) enhances γH2AX and 53BP1 foci formation, suppresses RAD51 foci, and impedes replication fork progression compared to chemotherapy alone, thereby impairing homologous recombination repair (HRR). Here, ATR is linked to ovarian cancer.