This way, immunological tolerance is maintained toward self‐antigens,[39] a mechanism being exploited by tumor cells to evade anticancer immune responses.[40] If apoptosis, however, occurs in a highly pro‐inflammatory context, T‐cell co‐stimulation by activated DCs drive antitumor responses critical in the inactivation of cancer cells.[41] CRT and heat‐shock proteins are two key immunological determinates in this context,[42, 43, 44] and our results underline their increased surface expression in the immunogenic treatment regimens mitoxantrone (MTX) and gas plasma treatment. Here, CALR is linked to cancer.