TGFB1 and neoplasm: Due to the modest antitumor activities of unmodified NK cell infusion, various strategies have been developed in the past few years to improve NK cell recognition and activation, including overexpressing chemokines or chemokine receptors to enhance NK cell tumor infiltration (112, 113), concurrent use of immune checkpoint inhibitors to reverse NK cell exhaustion (114), blocking the immunosuppressive TGF-β signaling from the TME (115), and promoting NK cell tumor-specific engagement through NK cell engagers (NKCEs) (31, 116–119).