As explained earlier, in some studies the aberrant expression and activation of other receptor tyrosine kinase and downstream cell signalling molecules (e.g. IGF-1R, c-Met, Src) have been shown to co-operate with HER family members to drive tumour growth and to confer resistance to therapy including treatment with HER inhibitors23–26, 31, 32. Here, NTRK1 is linked to neoplasm.