Down regulation of SOD2 expression would be expected to compromise this important mitochondrial protection mechanism and combined with small molecule Trk inhibitors and agents that promote mitochondrial ROS production, could increase TrkAIII-expressing tumour cell-sensitivity to mitochondrial ROS-mediated death and may also target the tumour stem cell-niche, which is promoted by TrkAIII and associated with enhanced SOD2 expression [49]. The gene discussed is SOD2; the disease is neoplasm.