PDCD1 and glioblastoma: In particular, the hypoxia environment resulted from bevacizumab treatment may upregulate PD-L1 expression in tumor cells and PD-1 expression in CD8+T cells, leading to effector T cell exhaustion and tumor regrowth (Figure 2C).50 This has led to the combination strategy of using immune checkpoint inhibitors to improve the bevacizumab efficacy for treating GBM patients (NCT03890952).