It is also possible that glioblastoma cells exploit IFN- γ through low level upregulation to induce PD-L1 expression and escape immune cell detection.82 These factors may help to explain why these early immunotherapeutic approaches were disappointing,83 and why current focus has moved towards therapies that either prime immune cells to target-specific tumour-associated antigens, or modulate the TME to reverse immune escape (Fig. 2). This evidence concerns the gene CD274 and glioblastoma.