For instance, combining bortezomib, a specific inhibitor of 26S proteasome, which causes tumor cell death and also stimulates antitumor immunity, with siRNA-mediated melanoma antigen gene member C1 (MAGE-C1) knockdown—MAGE-C1 is a member of cancer-testis antigens (CTAs), a group of tumor antigens—was reported to increase cell sensitivity to the first immunotherapeutic approach (bortezomib) in multiple myeloma cell lines [79]. The gene discussed is MAGEC1; the disease is AL amyloidosis.