The present study revealed the following main results: (i) Trk inhibitor [18F]TRACK is taken up into TrkA expressing human KM12 colon cancer cells, and this uptake can be inhibited by pan-Trk inhibitor entrectinib; (ii) [18F]TRACK is also taken up into KM12 tumor tissue as well as brown adipose tissue (BAT) in vivo which can also be blocked by entrectinib; and (iii) amitriptyline acts as a functional Trk agonist and increases uptake of [18F]TRACK in peripheral target tissue. This evidence concerns the gene TPM3 and colonic neoplasm.