Since our data proved that TNFRSF14 activates FAK/NF-κB axis to promote malignant phenotypes of GBM cells, we sought to examine whether TNFRSF14 affected CXCL1 and CXCL5 secretion in GBM cells through FAK/NF-κB activation. This evidence concerns the gene PTK2 and glioblastoma.