In addition, several lines of evidence, including activation and translocation of proapoptotic Bax from the cytoplasm to mitochondria, cytochrome c release from mitochondria to the cytoplasm, and cascade activation of caspases-9, -3, and -6, also showed that the enzalutamide-induced death mechanism in human drug-sensitive and -resistant glioblastoma cells occurred through an apoptotic pathway. This evidence concerns the gene BAX and glioblastoma.