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]. This evidence concerns the gene PMAIP1 and AL amyloidosis.