Corroborating this, treatment with a PARP inhibitor also partially blocked cytochrome c release from the mitochondria into the cytosol in this study (Figure 2c); therefore, PARP1 might regulate both caspase-dependent/independent cell death via proapoptotic Bcl-2 family protein activation in NPe6-PDT-dependent GBM cell death. Here, BCL2 is linked to glioblastoma.