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. Here, NGLY1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.