In recent years, the broadened understanding of the interplay between components of the immune system and malignant cells has paved the way for establishing powerful tools of immunotherapy in the clinics. One major goal of cancer immunotherapy is to stimulate tumor-reactive T cells, which are often silenced in the tumor microenvironment. Molecules related to tumor escape from T-cell attack include cytotoxic T lymphocyte-associated protein-4 (CTLA-4) and programmed death-1 (PD-1), which are upregulated on T cells as a counter-regulatory mechanism upon prolonged stimulation . The interaction of these “immune checkpoint” molecules with their ligands, B7.1/B7.2 and PD-L1/PD-L2 expressed on antigen-presenting cells and tumor cells, respectively, inhibits positive signals mediated by the T-cell receptor (TCR) or the costimulatory receptor CD28 and thereby leads to suppression of T-cell responses [2–5]. Therefore, antibody-mediated blocking of immune checkpoints is an effective approach to boost tumor-reactive T-cell functions.