HMGB1 and neoplasm: MyD88 KO mice have defects in TLR signaling and our results show that zVAD-fmk did not further retard growth of B16 tumors treated with RT, DTIC and HT in these mice (Figure 5b), again indicating that HMGB1 in vivo is a key player in zVAD-fmk-induced anti-tumor immune responses.