Moreover, it has been reported that ROS is a potent activator of JNK through oxidative inactivation of endogenous JNK inhibitors, such as JNK phosphatases and glutathione S-transferase π. 19 The results of the present study indicated that sustained activation of the JNK pathway (e.g., phosphorylation of JNK and c-Jun) was induced by DS/Cu in leukemia stem-like cells while reversed by NAC that inhibited ROS production, supporting a notion that ROS-activated JNK signal might be, at least in part, responsible for DS/Cu-induced apoptosis. This evidence concerns the gene JUN and leukemia.