Specifically, the elevated ROS generated by SCD1 inhibition damages mitochondria and activates the pro-apoptotic Bcl-2-associated X protein (BAX); activated BAX then promotes cytochrome c release, which in turn initiates the mitochondrial apoptotic pathway and activates caspase-9, ultimately leading to tumor cell death and thereby suppressing tumor metastasis [54, 55]. Here, CYCS is linked to neoplasm.