Four principal mechanisms mediate aberrant activation of receptor tyrosine kinase (RTK) in human cancers: autocrine activation, chromosomal translocations, overexpression, or gain-of-function mutations [122] and activation of signals by overexpression of oncogenes including RAS, RAF, and MYC would result in correspondingly increased tumorigenicity of cancer cells [123]. The gene discussed is NTRK1; the disease is cancer.