We examined the selective cancer cell-killing effect of a specific SOD1 inhibitor (LD100) that serves as a copper-chelated agent from the modulation view of the ROS signaling network, revealing that this effect of LD100 can be attributed to the SOD1 inhibition-mediated repression of the ROS signaling pathways to promote maintenance of cancer cell growth and the activation of the ROS pathways to trigger cycle arrest and apoptosis of cancer cells, not normal cells. The gene discussed is SOD1; the disease is cancer.