Because enforced TrkB expression promotes the metastatic capacity of lung adenocarcinoma [44] and is sufficient to suppress apoptosis, tumor formation, and metastasis in an animal model [45, 46], it appears beneficial that PTX3-induced upregulation of TrkB rather than BDNF allows PTX3 to remain responsive to BDNF stimulation. The gene discussed is BDNF; the disease is neoplasm.