KLRK1 and neoplasm: Knockdown of TGFBR2 or SMAD3 in NK cells, engineering CB NK cells to express TGF-β dominant negative receptor II, or modifying NK cells using CAR containing TGF-β type II receptor extracellular and transmembrane domains, and the intracellular domain of NKG2D, are all under investigation and have shown great promise for the recovery of tumor-suppressed NK cell antitumor activity to treat patients with solid tumors (129–131).