It is noteworthy that these pro-survival signaling pathways (e.g., NF-κB and Nrf2), as well as the stress-related ROS-JNK pathway, are determinants for tumor cell survival versus death in a variety of cancers.39, 40, 41, 42, 43, 44, 45 Thus, inactivation of NF-κB and Nrf2 signals and/or activation of the ROS-JNK signaling cascade might represent common mechanisms of action underlying the antitumor activity of DS/Cu in diverse cancers, including hematologic malignancies (e.g., myeloid and lymphoid leukemias) as we observed earlier.19, 46. This evidence concerns the gene NFKB1 and hematologic disorder.