These therapeutic approaches are focused on improving cancer patients’ NK cell effector functions by inducing their activation with cytokines or with bi/tri/tetra-specific killer cell engagers and/or on preventing NK cell inhibition with immune-checkpoint inhibitors, such as monalizumab that blocks the inhibitory receptor CD94/NKG2A (hereafter NKG2A) (6, 10, 11). The gene discussed is KLRC1; the disease is cancer.