To explain the antitumor role of TGF-β in our study, the binding of TrkC by the ligated conjugates might have activated the tyrosine kinase activity of TrkC and subsequently blocked the TGF-β signalling and inhibited TGF-β production at an early time point, which in turn reduced the Treg cells in a late time point to overall delay the tumor growth. This evidence concerns the gene NTRK3 and neoplasm.