Indeed, it has been found that increased ILT2 expression engaging HLA-G contributes to the dysfunction of CD56dimCD16+NK cells [117] and that a tumor-expressing HLA-G promotes the accumulation and suppressive activities of immune cells such as Treg and mast cells, as well as converting NK cells, T-cells and macrophages toward a pro-tumor phenotype [118]. This evidence concerns the gene LILRB1 and neoplasm.