Under conditions of a prolonged, strong checkpoint arrest when mitosis is dramatically disrupted by a failure to form the mitotic spindle, for instance due to the action of a cancer chemotherapeutic microtubule poison, the steady rate of Mcl‐1 destruction would still result in apoptosis once a threshold level was reached because its degradation is insensitive to the checkpoint even though the rate of degradation of cyclin B1 and other mitotic APC/C substrates that hold a cell in mitosis is reduced (Fig 7A, right). Here, MCL1 is linked to cancer.