While it is clear that in the presence of specific cytokines, the interaction between Tim-3 and Gal-9 results in enhanced IFN-γ production by CD56bright NK cells, it remains to be elucidated whether engagement of Tim-3 triggers NK cell activation and how NK cell function is modulated by changes in Tim-3 expression in the context of viral infections. This evidence concerns the gene HAVCR2 and viral infectious disease.