This novel TrkAIII/SOD2 axis function suggest that the combined use of TrkAIII and/or SOD2 inhibitors, together with radiotherapy or chemotherapeutic agents that induce mitochondrial free radical ROS-mediated death, could provide a therapeutic advantage that may not only enhance tumour cytotoxicity but may also reduce malignant behaviour and target the stem cell niche in high TrkA expressing unfavourable NBs. The gene discussed is NTRK1; the disease is neoplasm.