To be certain that BTZ mediated abrogation of autophagic flux was responsible for the biological effects on GBM cell death during combination treatment with TMZ, colony formation as an indication of clonogenic survival was monitored in P3 and T98G cells depleted of ATG5 or ATG7, or treated with MRT68921 (ULK1/2 inhibitor) or VPS34-IN1 (VPS34 inhibitor) under steady state and during BTZ and TMZ treatment. The gene discussed is CASC3; the disease is glioblastoma.