These effects associate with increased mitochondrial capacity to produce H2O2, occur within the context of a more tumour stem cell-like phenotype, and can be reversed by the specific TrkA tyrosine kinase inhibitor GW441756 [51], by the multi-kinase TrkA inhibitors CEP-701 [59], K252a [49] and Gö6976 [50] and by siRNA knockdown of SOD2 expression, all of which restore the sensitivity of TrkAIII SH-SY5Y cells to Rotenone, Paraquat and LY83583-induced mitochondrial free radical accumulation and free radical-mediated death. The gene discussed is NTRK1; the disease is neoplasm.