Moreover, the receptor tyrosine kinase mesenchymal–epithelial transition factor (MET) is notably upregulated within the TME of secondary GBM, and has been shown to initiate the STAT4–PD-L1 signaling cascade in primary GBM, thereby enhancing GAMs infiltration and contributing to immune escape mechanisms (25, 26). This evidence concerns the gene CD274 and glioblastoma.