ATM and cancer: Previous studies have reported that high endogenous ROS levels correlate with the activation of the JNK pathway and DNA damage response in human cancer cells [33, 34]; ROS-mediated JNK activation–induced DNA damage causes mitochondrial dysfunction-related apoptosis [35]; and ATM, which is well known for its role in the cellular response to DNA breaks, also regulates many diseases through JNK [36].