Together, these data suggest that the potentiation of sub-toxic DSF activity against human melanoma and breast carcinoma cells irrespective of their BRAF or p53 mutant status and EGFR2/HER2 over-expression, is not merely related to Cu sequestration or increased Cu uptake by Cu chelators or ionophores, but rather to the ability of low DSF levels to increase basal Cu-dependent generation of ROS through higher intracellular hydroxyl radicals (•OH) production [19], since it is attenuated by the Cu chelator TTM or by the anti-oxidant NAC (Summary, Figure 6). The gene discussed is ERBB2; the disease is breast carcinoma.