Tumor cells can employ a plethora of mechanisms to induce NK cell dysfunction, including upregulation of immune checkpoint expression, such as PD-1, prolonged exposure to MHC class 1-deficient tumor cells and/or NK cell activating receptor antagonists [82,83], the secretion of tumor cell-derived exosomes [84], as well as the secretion of inhibitory tumor-derived cytokines, such as IL-10 and TGFβ1 [66,85,86]. The gene discussed is NCR1; the disease is neoplasm.