NRF1 and hematopoietic and lymphoid cell neoplasm: Taken together, these findings suggest that crippling the NRF1-mediated bounce-back response can both potentiate CFZ-induced apoptosis in hematologic cancers that already respond well to proteasome inhibition and may even sensitize previously non- or minimally-responsive tumors (e.g., solid tumors) to proteasome inhibition (reviewed in [7]).