STAT3 activation in GBM is driven by multiple receptor tyrosine kinase pathways, including the EGFR, PDGFR, and c-MET pathways, along with the loss of negative regulators such as protein tyrosine phosphatases, suppressors of cytokine signaling, and protein inhibitors of activated STAT3.276 This sustained activation promotes tumor growth by upregulating the expression of oncogenic transcription factors such as c-Myc, cyclin D1, and Bcl-xl. This evidence concerns the gene NTRK1 and glioblastoma.