Most importantly, this failure to increase autophagosome formation under BTZ treatment in ATG5 and ATG7 knockout P3 and T98G cells rescued them from death by treatment with BTZ alone or in combination with BTZ + TMZ in vitro. This in vitro finding translates in vivo in mice with reduced survival of P3 ATG5−/− implanted mice where combination treatment no longer effectively killed the GBM cells, indicating that cell death induced by BTZ is robustly dependent on a functional autophagy machinery. The gene discussed is ATG5; the disease is glioblastoma.