Through the more benign setting of HCMV infection, we demonstrate that the maturation of adaptive NK cells and the execution of NK cell function can be modulated by the Tim-3 pathway as its engagement, whether directly through Ceacam-1 and Galectin-9 or indirectly after activation alters the adaptive phenotype of NK cells. This evidence concerns the gene HAVCR2 and cytomegalovirus infection.