A theoretical model for how proteasome inhibitors could affect the balance between pro- and antiapoptotic forces in MCL. Proteasome inhibition leads to increased NOXA and MCL-1, the latter of which could theoretically mitigate some of the therapeutic merit of targeting the proteaseome. However, the selective increase in NOXA results in liberation of the pro-apoptotic BAX, which then mediates induction of apoptosis.