Tumoral immune resistance is very complex and involves different mechanisms, such as tumor mutational burden leading to insufficient tumor immunogenicity, irreversible T-cell exhaustion, MHC (Major Histocompatibility Complex) dysfunction, and an immunosuppressive tumor microenvironment (TME), notably through the recruitment of MDSCs (Myeloid Derived Suppressor Cells) [5,6,7,8,9]. This evidence concerns the gene HLA-C and neoplasm.