Yu’s group has previously demonstrated that STAT3 activation shuts down the innate immune-stimulating molecules such as interferon γ induced by CD8+ T cells, pro-inflammation cytokines (IL-12, tumor necrosis factor-α) and chemokines (C-C Motif Chemokine Ligand 5 (CCL5), C-C Motif Chemokine Ligand 9 (CCL9)), and suppresses the maturation of dendritic cells via secreting tumor-associated factors such as IL-6, IL-10, VEGF which in turn activate STAT3 in a positive feedback loop [111]. The gene discussed is CD8A; the disease is neoplasm.