With the above-mentioned knowledge as the starting point, here we examined potential mechanistic links between cancer-associated replication stress, DNA damage checkpoint signaling and the functional impact of DSF/CuET treatment on DNA replication and genome integrity maintenance, searching for possible explanations of the overall sensitivity of tumor cells, and the observed preferential sensitivity of cancer cells lacking BRCA1 and BRCA2, to treatment with DSF/CuET. The gene discussed is BRCA1; the disease is neoplasm.