Having identified changes in the activity of the central apoptotic mediator caspase 3, which is a downstream target of UPR signaling and inhibitor of poly ADP ribose polymerase (PARP), we subsequently also analyzed the cleavage of PARP and tested whether the therapeutic PARP-inhibitor olaparib affects CML cell death in combination with TKIs. The gene discussed is CASP3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.