After observing the functional role of FAK/ FAK Y397 phosphorylation induced by cancer intrinsic TNFRSF14 in promoting malignant progression of GBM (Fig. 4), we sought to validate the association between FAK/ FAK Y397 phosphorylation induced by TNFRSF14 and TAMs infiltration in clinical GBM samples. This evidence concerns the gene PTK2 and glioblastoma.