Transcription factors regulated via IFNs such as IRF1 and IRF3 have been reported to promote upregulation or activation of Puma and Bax.26, 27 Puma and Bax were also described as DNA damage-induced target genes that are upregulated by TMZ treatment.28 Consistently, we show in the present study that IFNβ and TMZ cooperate to upregulate Puma and Bax, which both contribute to BV6/TMZ-induced apoptosis, as genetic silencing of either Bax or Puma, two Bcl-2 family proteins known to promote mitochondrial apoptosis, rescues glioblastoma cells from cell death. The gene discussed is BAX; the disease is glioblastoma.