Collectively, these observations strongly suggest that oncogenic alternative TrkAIII splicing represents a frequent alternative to TrkA-fused oncogenes in different tumor types, which is consistent with the recognition that alternative splicing is an oncogene activation alternative to gene mutation in a wide variety of cancers, and in particular, tumors with low mutational burdens [30,31,32]. This evidence concerns the gene NTRK1 and neoplasm.