ATG5 and central nervous system cancer: ,75,76 Recent observations have indicated that NF-κB-triggered JNK activation promotes apoptosis and inflammation, supporting rNDV-F0-GFP proliferation and validating the GO terms “IRE1-mediated unfolded protein response” and “I-kappaB kinase/NF-κB signaling.”77,78,79 In addition to those terms, the gene ATG5 significantly correlated with PBT sensitivity to rNDV-F0-GFP, aligning with previously reported siRNA silencing of ATG5 affecting NDV production in U251 glioma cells.80