The restricted expression pattern of HLA-G has meant that its transcriptional regulation has been difficult to study, with data almost exclusively based on cancer cell lines and/or overexpression studies which collectively demonstrate many regulatory elements—including interferon-stimulated response element (ISRE) which can be activated by interferon-γ (IFN-γ), one of the most potent inducers of MHC class I proteins—on the proximal promoter of HLA-G are largely non-functional [22,23,24]. This evidence concerns the gene HLA-G and cancer.