In this phase, as in the priming phase, the anti-tumor response is controlled by immune checkpoints and can be suppressed by the activation of inhibitory co-receptors of the lymphocyte, such as programmed cell death receptor PD1, due to the interaction with immune-suppressive proteins expressed by tumor cells and cells from the tumor microenvironment (TME), such as PD1 ligand PDL1- [40]. The gene discussed is CD274; the disease is neoplasm.