Entrectinib use is currently restricted to cancers driven by Trk fusion oncogenes, for which it exhibits profound, durable efficacy [13], supporting calls to extend clinical Entrectinib approval to refractory, advanced-stage metastatic NBs that exhibit TrkAIII expression and activation, bolstered also by evidence that TrkAIII behaves as an oncogenic equivalent to the TrkT3 fusion oncogene in NB models [6] and alternative splicing is a frequent oncogenic pathways activation mechanism in tumors, such as NBs, that exhibit low gene mutation rates [14,15,16,17]. This evidence concerns the gene NTRK1 and neuroblastoma.