Our data demonstrated by a molecular biological approach that apoptosis of ROS1-TKI–addicted cells by excessive ROS1 signaling seemed to be strongly dependent upon caspase-8 and molecules related to death receptor-dependent apoptosis rather than on caspase-9 and molecules related to apoptosis originating from the mitochondria, suggesting that the apoptotic mechanism induced by excessive ROS1 signaling differs from that caused by high concentrations of ROS1-TKIs during cancer treatment. The gene discussed is ROS1; the disease is cancer.