Although previous reports show that the activation of TrkA by its cognate ligand, β-NGF, promotes the phosphorylation of STAT3 on its Y705 and S727 residues and promotes STAT3 transcriptional activity, the co-activation of JAK2–STAT3 and TrkA signaling pathways, and the mechanisms underlying their crosstalk, have never been investigated in any cell or tumor type [27,28]. The gene discussed is JAK2; the disease is neoplasm.