TIGIT and neoplasm: This could be achieved by masking tumor checkpoint ligands [i.e., anti-PD-L1, Avelumab, which can also initiate NK cell ADCC (69, 120, 169, 261, 278, 279), or the TIGIT ligands CD112/CD155 (105, 280, 281)], activating NK cells in-situ with cytokine variants, and modulating tumors via bio-chemical modifications or inhibitors, making them more susceptible to NK cell-mediated lysis.