It is now well established that CMV infection or reactivation can reduce the risk of relapse after HSCT by enhancing NK cell maturation with increased CD56dim population, shaping NK cells toward an activated phenotype with upregulation of NKG2C (activation) and KIR receptors and downregulation of NKG2A (inhibitory) along with increased expression of CD57, and creating “memory NK cells” (106–112). This evidence concerns the gene KLRC1 and cytomegalovirus infection.