We recently described the upregulation of HLA-E in ovarian and cervical cancers. Instead of interacting with natural killer cells, HLA-E appeared to inhibit intratumoral cytotoxic T lymphocytes (CTL) via the receptor CD94/NKG2A. Strikingly, the survival benefit of intraepithelial infiltrating CTL was lost in those cancers with high HLA-E expression.