As discussed below, this is mainly because of the lack of tumor-specific antigens (TSAs) and neoantigens [36,37,38], low expression of the classical human major histocompatibility complex class I (MHC-I) and thus impaired MHC-peptide presentation [39], upregulation of checkpoints and the immunosuppressive tumor microenvironment (TME), which is mostly populated by pro-tumorigenic M2 macrophages. Here, HLA-C is linked to neoplasm.