NTRK1 and neoplasm: Collectively, these observations support a potentially frequent and actionable role for alternative TrkAIII splicing as an oncogenic alternative to TrkA-gene fusion in different tumor types, consistent with a report that alternative splicing is a significantly frequent oncogene activation mechanism in a wide variety of tumor types [30] and in particular tumors with low mutation burdens, such as NBs, MCPyV-positive MCCs, PRCs, GBMs, and MTCs [30,31,32].