Mps1 is activated on the kinetochore to assembly MCC, allowing tumor cells to keep a basic level of the SAC to maintain genome instability; meanwhile, another fraction of active Mps1 is recruited to mitochondria by binding to VDAC channels that inhibits the release of cytochrome c and eventually prevents aneuploid tumor cells from dying from various stresses. Here, CYCS is linked to neoplasm.