Consistent with our results, JS‐K down‐regulated SOD1 expression in human leukaemia HL‐60 cells in a previous study.43 The disruption of reductase antioxidant systems, including SOD1, catalase or GSH peroxides, is well known to contribute to ROS‐dependent cytotoxicity for some chemotherapeutic agents.24, 26 Therefore, the suppression of antioxidant enzyme activation might be another mechanism by which JS‐K induces ROS accumulation. The gene discussed is SOD1; the disease is leukemia.