Mechanisms involved in tumor immune evasion can be diverse and include upregulation of the non-classical MHC molecules HLA-E and HLA-G that trigger inhibitory NK-cell receptors (9), selective loss of ligands for activating NK-cell receptors (10, 11), as well as shedding of soluble forms of MHC class I polypeptide-related sequence A/B (MICA/B) and B7-H6 (12–14). This evidence concerns the gene HLA-G and neoplasm.