HMGB1 and neoplasm: The latter, acting as a sort of “super‐alarmin” would trigger, in an endoplasmic reticulum stress‐dependent manner, the exposure of damage‐associated molecular patterns (including cell surface CRT, ATP, HMGB1, HSP70 and HSP90) resulting in the recruitment and activation of APCs and activation of the anti‐tumor T cell immune response, thus eliciting an immunogenic cell death response.106