Emerging evidence reveals that NTRK1 signaling induces distinct transcriptional programs across pathologies [34]—in glioblastoma, NTRK1 complexes drive Insulin-Like Growth Factor II (IGF2) expression to promote tumor survival [15], while, in neuropathic pain, NTRK1- cAMP responsive element binding protein (CREB) signaling upregulates matrix metalloproteinase-9 (MMP9), disrupting blood–nerve barriers [37,38]. The gene discussed is IGF2; the disease is neoplasm.