Glioblastoma cells overexpress the voltage-dependentanion channel 1 (VDAC1), which is crucial for energy metabolism, controlsmitochondria-mediated apoptosis through engaging with antiapoptoticproteins, and inhibits glioblastoma cells death.59 Shteinfer-Kuzmine et al. developed VDAC1-targeting peptidesthat inhibited the anti-apoptotic activities of these proteins, activatedmitochondria-mediated pathways, and initiated apoptosis. The gene discussed is VDAC1; the disease is glioblastoma.