Mechanistically, cancer intrinsic TNFRSF14 phosphorylates FAK at Y397 and activates its downstream NF-κB signaling, which not only enhances the tumorigenicity of GBM cells, but promotes the recruitment of anti-inflammatory TAMs through elevating CXCL1 and CXCL5 secretion from GBM cells. This evidence concerns the gene CXCL5 and glioblastoma.