Recently, Chiba et al. (10) reported that tumor-infiltrating DCs show increased Tim-3 expression and suppress nucleic-acid-mediated innate immune responses as a result of the interaction between Tim-3 and the alarmin HMGB1, and that, when Tim-3 signaling was blocked using anti-Tim-3 monoclonal antibody, chemotherapy was found to be more effective, suggesting that Tim-3 plays a role in tumor pathogenesis. The gene discussed is HAVCR2; the disease is neoplasm.