Studies have found that a histone deacetylase inhibitor such as panobinostat induces apoptosis in hepatocellular carcinoma associated with up-regulation of ER stress markers (Grp78, eIf2a, and XBP-1).[29] Treatment of chronic lymphocytic leukemia and multiple myeloma cells with brefeldin A, an inhibitor of ER to Golgi protein transport cause a decrease in VEGF secretion and abnormal ER swelling; and subsequently activation of caspases, and cell death.[30] UPR is an intricate process in the face of cellular ER stress. This evidence concerns the gene XBP1 and AL amyloidosis.