Its most efficient ligand is a dimerized HLA-G which was described as up-regulated in some human tumors such as breast cancer (Lefebvre et al., 2002), certain AML (acute myeloid leukemia) (Kang et al., 2015) and cutaneous T cell lymphoma (Urosevic et al., 2004) in which both CD8+ T and CD56+ NKT cells highly expressed LILRB1 and thereby possibly contributed to tumor immune escape. This evidence concerns the gene LILRB1 and breast carcinoma.