NTRK1 and neoplasm: This leads to the survival of resistant tumor cells and an increase in the number of mutations [e.g., in HER2, BCL-2, signal transducer and activator of transcription 3 pathway (STAT3), B-RAF proto-oncogene, serine/threonine kinase (BRAF), epidermal growth factor receptor (EGFR), tyrosine-protein kinase KIT (KIT) genes]; applicable therapeutic strategies include targeting oncogenes and tyrosine kinase receptors e.g., BRAF inhibitors or anti-HER2 antibodies, small molecules, antibody-drug conjugates, and vaccines.