Several factors have been identified within the TME, such as a genetic and epigenetic mutational load that controls neoantigen processing or presentation by the tumor cells, inhibitory checkpoint expression (e.g., PD-L1) and activation of oncogenic signaling pathways (tumor cell intrinsic mechanism) that suppress the therapeutic effects of ICB by disrupting the functions of tumor-specific cytotoxic T cells [2,7]. The gene discussed is CD274; the disease is neoplasm.