In the present studies, treatment of GBM cells with PBI-05204 significantly increased caspase 3–dependent apoptosis which results from a mixture of mitochondrial damage (mitochondria pathways and intrinsic apoptosis), with caspase 9 activation, and death receptor mediated cell death with caspase 8 activation (extrinsic pathway of apoptosis). This evidence concerns the gene CASP3 and glioblastoma.