Furthermore, there is preclinical evidence of synergy between venetoclax and conventional anti-myeloma therapies such as dexamethasone and proteasome inhibitors, which have been shown to upregulate BIM and the MCL1 selective BH3-only protein NOXA, respectively, thereby increasing dependence on BCL2 in myeloma cell lines and primary cells [118–121]. The gene discussed is PMAIP1; the disease is plasma cell myeloma.