Reactive oxygen species accumulation usually leads to oxidative stress and DNA damage, which then activate c‐Jun N‐terminal kinase (JNK) and initiate apoptotic cell death.26, 31 Consistent with this concept, ROS accumulation and the subsequent JNK activation mediate JS‐K‐induced cell death and growth arrest in human hepatoma,32 NSCLC33 and multiple myeloma cells.6, 34 As many kinds of chemotherapeutic drugs, including arsenic trioxide and cisplatin, also exert their anti‐cancer activities by facilitating ROS accumulation,11 JS‐K is a promising anti‐cancer drug with a similar mechanism. This evidence concerns the gene MAPK8 and plasma cell myeloma.