After exposed to RT, HMGB1 was passively released from dying tumor cells into extracellular space and acted as a DAMP.25 Then, TLR4 on the surface of DCs binds to HMGB1 and initiates the antitumor immune response.26 Considering that ERAD inhibitors synergized with RT were able to trigger an enhanced tumor cell death, we wished to assess whether ERAD inhibitors could be utilized to promote HMGB1 release in EC cells. Here, HMGB1 is linked to neoplasm.