In pancreatic cancer, we have demonstrated the effectors functions of antigen specific Th1/Th17 Tcc (40) supporting the theory that, when Th17 turn into IFN-γ-expressing Th17 (Th17/Th1 cells), they can contribute to protective antitumor immunity, eradicating tumor cells through production of IFN-γ, or inducing Th1-type chemokines and stimulating CXCL9 and CXCL10 production to recruit effector cells to the tumor microenvironment (39, 41, 42). The gene discussed is CXCL10; the disease is pancreatic neoplasm.