Previously, we revealed that conventional anti-myeloma medicines such as the proteasome inhibitor carfilzomib, the BCL-2 inhibitor venetoclax, or the HDAC inhibitor Na-valproate induce an intensive, bidirectional transfer of functional mitochondria between bone marrow stromal cells and MMs, which provides remarkable resistance to these pharmaceuticals for the malignant plasma cells. The gene discussed is BCL2; the disease is plasma cell myeloma.