Since there is no known HLA-G receptor (such as ILT2, ILT4 or KIR2DL4) present on the tumor cells used in this study and given the large number of interacting physiological ligands and receptors that can come into play in a cell [49], it might be conceivable that these cells possess not yet characterized receptors, that might act in concert with HLA-G responsible for the modified tumor response. This evidence concerns the gene HLA-G and neoplasm.