Anticancer therapeutics can inhibit suppressive mechanisms of tumor-induced immune tolerance (blue circle), boost T and/or B cell responses (pink circle), or stress tumor cells in such a way that tumor cells become immunogenic and sensitive to lysis (yellow circle). The main drugs driving these effects are also shown. Cyclophosphamide at low doses, gemcitabine, and all-trans-retinoic acid (ATRA) act on immunosuppressive cells such as Tregs or myeloid suppressor cells (MdSC) to facilitate tumor attack by conventional effectors (Tconv). Pharmacological inhibition of MdSCs can also be achieved by nitroaspirin (96), sildenafil (97), and biphosphonate (98). Androgen deprivation boosts T and B cell responses. Strategies leading to lymphodepletion allow the establishment of memory effector T cells efficient in long-term protection against tumor cells. Tyrosine kinase inhibitors boost DC/NK cell crosstalk. The proteasome inhibitor bortezomib induces myeloma cell–surface expression of the molecular chaperone protein HSP90, which leads to DC uptake, antigen processing, and DC maturation. Anthracyclines, oxaliplatin, and irradiation promote tumor membrane expression of CRT and release of HMGB1 by tumor cells, which are required events for DC-mediated phagocytosis of dying tumors and cross-presentation of tumor antigens to T cells, respectively. Inhibitors of histone deacetylases (HDACs) promote the expression of NKG2D ligands (NKG2DL), sensitizing the tumor cell to NK cell–mediated lysis. Tumor cells exposed to x-rays express increased numbers of MHC class I molecules, tumor antigens, and Fas, favoring CTL attack. Flavanoid-mediated production of chemokines favors attraction of immune effectors into tumor beds. Ideally, an appropriate combination of chemotherapeutic agents could achieve all of these three types of beneficial effects.