Reports indicated that the release of endogenous danger signals, such as high-mobility-group box 1 (HMGB1), caused by chemotherapy-mediated tumor cell death, can stimulate DC cross-priming in a TLR-4/MyD88-dependent manner [17] and induce robust innate immune responses and antibody-mediated tumor regression [12]. The gene discussed is MYD88; the disease is neoplasm.