Despite the complex interactions realized in the immunological synapses between cytotoxic T lymphocytes (CTLs) and target cells [7,8], the selective activation of anti-tumor T cells reside in the balanced affinity between the T cell receptor (TCR) and the molecular target complex of tumor associated antigen (TAA) peptides bound to the MHC products (pMHC) on the targeted tumor cells. This evidence concerns the gene HLA-C and neoplasm.