Functional assays demonstrated that IFNGR2 knockdown suppressed glioma cell proliferation and attenuated NF-<i>κ</i>B signaling, underscoring its role as a key driver within the TRP network.<h4>Discussion</h4>TRPRS provides a robust, biologically grounded tool for simultaneous prognostication and therapy guidance in GBM, highlighting TRP signaling as a therapeutic vulnerability. The gene discussed is IFNGR2; the disease is central nervous system cancer.