Adoptive transfer of large numbers of cytotoxic UCB-NK could be a viable treatment option, because UCB-NK have a highly activated phenotype with more than 75 % stable expression rates of NKG2D, DNAM-1, NKp30, NKp44 and NKp46 in all mature UCB-NK, and lack inhibitory KIRs, resulting in HLA-independent cytolytic efficacy; additional advantages of UCB-NK over PBNK are fewer impurities (such as T and B cells) detected upon full NK maturation, thereby reducing chances of GVHD upon adoptive transfer [30, 36]. The gene discussed is KLRK1; the disease is graft versus host disease.