Targeting CD94/NKG2A rather than HLA-E molecule with antagonist molecules could be key to unlock the CD94/NKG2A-mediated inhibition and to preserve the CD94/NKG2C positive signaling in cytolytic lymphocytes (CD8 T cells, NK cells, and NKT cells) infiltrating ovarian cancers. The gene discussed is HLA-E; the disease is ovarian carcinoma.