As IL-15C treatment in vivo upregulates the expression of genes known to promote antitumor NK cell responses such as Perf1, Stat5a, Zeb2, Fcgr3, and Itga2a [59–63], while downregulating checkpoint inhibitors like Lag3 and Tigit [64], it is plausible that Nr2f6-deficient NK cells exhibit enhanced efficacy during NK cell-mediated tumor immunosurveillance, due to their intrinsic elevation in Ncr1 expression. Here, TIGIT is linked to neoplasm.