Mechanisms by which this escape may occur include loss of tumor antigens, down regulation of histocompatibility locus antigens (HLA) from the tumor cell surface; altered tumor microenvironment that is immunosuppressive due to the recruitment of regulatory T cells (Tregs); myeloid-derived suppressor cells, tumor-associated M2 macrophages, and others (11–13); upregulation of inhibitory receptors (e.g., PD-1) on T cells; or upregulation of inhibitory ligands (e.g., PD-L1 or B7-H3) on stromal cells or tumor cells. This evidence concerns the gene CD276 and neoplasm.