CREB1 and non-small cell lung carcinoma: Although we did not determine whether AMRI-59 protects normal tissue from IR-induced damage or whole cell death is mediated by the ROS/caspase pathway in response to the AMRI-59/IR combination, data from the current study support a novel role of AMRI-59 as a radiosensitizer that promotes apoptotic death of NSCLC cells through activation of ROS-induced apoptosis and suppression of ERK/CREB-1 activities.