The activation of TNFRSF14/FAK signaling subsequently activates NF-κB complex and promotes the nuclear translocation of p65, leading to the enhanced tumorigenicity of GBM cells, as well as increasing their CXCL1 and CXCL5 secretion, which facilitates the constitution of immunosuppressive TME through recruiting anti-inflammatory TAMs. The gene discussed is CXCL1; the disease is glioblastoma.