Preclinical studies have shown that both glucocorticoid dexamethasone and the proteasome inhibitor bortezomib can increase BCL-2 dependence in multiple myeloma cells by shuttling proapoptotic proteins from MCL-1 to BCL-2, simultaneously reducing BCL-XL expression and MCL-1 activity through the up-regulation of noxa (PMAIP1) [64,65]. The gene discussed is MCL1; the disease is AL amyloidosis.