Within this context, we previously reported a pro-survival stress-adaptation and drug-resistance mechanism in human neuroblastoma (NB), characterized by alternative TrkAIII splicing of the neurotrophin receptor tropomyosin-related kinase gene NTRK1/TrkA, which results in the expression of the oncogenic TrkAIII receptor variant [6,7]. This evidence concerns the gene NTRK1 and neuroblastoma.