Constitutively active STAT3 signaling in transplantable tumor cell lines has been reported to decrease expression of proinflammatory mediators, while expression of a dominant negative STAT3 variant resulted in augmented expression of proinflammatory factors, including the chemokines CCL5 and CXCL10, which are functionally responsible for T cell recruitment [25, 26]. The gene discussed is CCL5; the disease is neoplasm.