It is generally accepted that successful anti-tumor immune responses following PD-1/PD-L1 blockade require reactivation and clonal-proliferation of tumor-specific T cells present in the tumor microenvironment (TME) and the differences in the outcome of cancer immunotherapy can be partially attributed to the heterogeneity of the tumor microenvironment [109,110]. Here, PDCD1 is linked to neoplasm.