T lymphocytes are central players of the adaptive anti-tumor immune response. Activation of T lymphocytes requires two signals: the first one is originating from the T-cell receptor after interaction with an antigen-derived peptide presented by major histocompatibility complex, while the second is delivered upon interactions between co-receptors on T cells and their ligands on antigen-presenting cells (APCs) or target cells . Co-receptors, also called immune checkpoints, can be divided into stimulatory and inhibitory molecules. The CD28 was the first identified co-stimulatory molecule and the interaction between CD28 and B7.1/B7.2 is one of the dominant pathways required for full activation of naive lymphocytes [2, 3]. In contrast, cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death 1 protein (PD-1), when interacting with their ligands B7.1/B7.2 and PDL-1/PDL-2 respectively, restrain the activation of lymphocytes T and are thus considered as co-inhibitory molecules [4–7].