As expected, we noticed that PD-L1-ex increased LC3B-II/I ratio, and decreased p62 expression levels to induce protective autophagy in TS-GBM cells treated with high-dose TMZ, and the effects of PD-L1-ex on TMZ-resistance in GBM cells were abrogated by co-treating cells with autophagy inhibitor 3-MA, suggesting that GSCs-derived PD-L1-ex activated autophagy to promote TMZ-resistance. The gene discussed is MAP1LC3B; the disease is glioblastoma.