Overall, these observations suggest a model in which active Ig-tagged soluble recombinant mLIGHT would act in a paracrine fashion on HVEM expressed on innate and adaptive immune cells- and/or on LTβR-expressing stromal, endothelial, and myeloid cells at a distance from the tumor site to trigger a local inflammatory response capable of interfering with tumor growth. The gene discussed is LTBR; the disease is neoplasm.