This could be driven by both cellular and molecular suppressive networks within the TME, but also within the tumor, such as e.g. the loss of tumor antigens, downregulated expression of HLA class I molecules and antigen processing machinery (APM) and interferon (IFN) pathway components as well as upregulation of various immune checkpoint (ICP) molecules, like PD-L1, B7-H4, B7-H6, LAG-3, TIM-3, VISTA, HLA-E or HLA-G (8–10). This evidence concerns the gene VTCN1 and neoplasm.