Next, the inhibitors for AMPK (compound C) and ULK1 (SBI-0206965) were used to inactivated AMPK/ULK1 pathway, and the results showed that both compound C and SBI-0206965 decreased LC3B-II/I ratio, and increased p62 levels to block autophagy in the TS-GBM cells co-treating with PD-L1-ex and high-dose TMZ (Fig. 5d–f), suggesting that PD-L1-ex activated AMPK/ULK1 pathway mediated autophagy in TMZ treated TS-GBM cells. Here, ULK1 is linked to glioblastoma.