In fact, CAR-NK cells still exert NK natural cytotoxic activity against tumor cells by the release of granzyme and perforin, for example, and can be activated via CAR-independent mechanisms, like natural cytotoxicity receptors (NCRs); NKp46, NKp44, and NKp30, NKG2D, co-stimulatory receptor; DNAX accessory molecule (DNAM-1), and specific activating KIRs (KIR2DS1, KIR2DS4 and KIR2DL4) [193, 194] which induce caspase-mediated apoptosis of targeted cancer cells. The gene discussed is KLRK1; the disease is neoplasm.