Using the EL4 tumor model, Maccubbin et al. [60] also showed that the anthracycline doxorubicin enhanced the cytotoxic T lymphocyte response, but it was more recently revealed that the mechanism of this immune modulation includes the translocation of calreticulin to the surface of tumor cells alerting DCs to take up dying tumor cells [20], the induction of heat shock proteins (Hsps) [61] and the secretion of high-mobility group 1 proteins [62]. This evidence concerns the gene HMGB1 and neoplasm.