Exhausted Tumor-associated (TA)-NK cells exhibit downregulation of effector cytokines, decreased degranulation potential, downregulation of activating receptors (such as NKG2D), upregulation of inhibitory receptors such as PD-1, TIM-3, T cell immunoreceptor with Ig, and Immunoreceptor Tyrosine-based inhibition Motif (ITIM) domains (TIGIT) and NKG2A and decreased expression of Eomesodermin and T-bet transcription factors (TFs) [13,14]. The gene discussed is KLRC1; the disease is neoplasm.