However, ligand-independent dimerization of receptor tyrosine kinases mediated by specific mutations in the kinase domain (Shan et al., 2012) or by overabundance of receptor tyrosine kinases (Wei et al., 2005) results in signalling activation and is a scenario well described in the context of cancer formation (Schlessinger, 2002). This evidence concerns the gene NTRK1 and cancer.