It is commonly assumed that the only goal of anticancer chemotherapy, like antimicrobial antibiotic therapy, is to eradicate by direct cytotoxic effects all tumor cells. According to this mechanism, complete and permanent cure would be obtained by antineoplastic agents that succeed in killing all cancer cells including cancer stem cells and micrometastases. 1, 2 In fact, cancer has long been conceived and treated as a cell-autonomous phenomenon, regardless of the immune system’s contribution to the therapeutic response. Recently, we have challenged this idea by showing that, at least in the case of anthracyclin-mediated chemotherapy, the antitumor immune response plays a major role in therapeutic success. Thus, immunocompetent mice bearing CT26 colon carcinomas or MCA205 fibrosarcomas can be cured by intratumoral injection of anthracyclins, whereas immunodeficient mice lacking T cells only exhibit partial responses with a delay in tumor growth. 3–5 Detailed molecular studies revealed that anthracyclins have the peculiar capacity of inducing immunogenic cell death. In contrast, many other cytotoxic agents including agents that damage nuclear DNA (such as etoposide and mitomycin C), mitochondria, the endoplasmic reticulum or lysosomes fail to induce immunogenic cell