The generation of an inflammatory and immune suppressive milieu in the TME induces tumor escape mechanisms, such as downregulation of classical HLA class I antigens and an upregulation of HLA-G and -E as well as iCPs including e.g., PD-L1 in the TME and CTLA-4 in the lymphoid tissues leading to evasion of adaptive immune responses (40–42). The gene discussed is HLA-G; the disease is neoplasm.