Notably, chemical inhibition of NGLY1 in chronic myelogenous leukemia and cervical cancer cells [18] or p97 in multiple myeloma cells [24] potentiated the apoptotic effect of proteasome inhibition, further strengthening the hypothesis that crippling the bounce-back response can increase the efficacy of PIs as cancer therapy. The gene discussed is NGLY1; the disease is plasma cell myeloma.