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). Here, CD274 is linked to neoplasm.