CHEK1 and cancer: When cell cycle is decelerated, via the treatment with UCN-01, the depletion of CHK1, pre-depletion of mitochondria, or blocking mitochondrial biogenesis by PGC-1α depletion, so that M-arrest is spared or attenuated, mitochondria will be more likely to stay homeostatic, thus generating less ROS and rendering cancer cells less responsive to the therapeutic agents.