In addition, tumor cells are able to increase the expression of non-classical HLA class I molecules (HLA-E and HLA-G), which can interact with the inhibitory receptors CD94/NKG2A and KIR2DL4/p49 on natural killer (NK) cells, as well as on effector T cells and myeloid cells (e.g., ILT2 and ILT4), leading to decreased NK cell and/or T cell effector activity and hereby potential tumor progression [7–11]. This evidence concerns the gene KIR2DL4 and neoplasm.