In MDS, high expression of TIGIT on NK and T cells correlates with decreased secretion of activation factors like CD107a, IFN-γ, and TNF-α, while blocking TIGIT enhances anti-tumor immunity.67 In pancreatic cancer, the CD155/TIGIT axis is co-opted to maintain immune evasion, as TIGIT modulates T cell exhaustion and dysfunction, with co-blockade strategies showing promise in reinvigorating tumor-reactive T cells.68 The presence of TIGIT on immune cells correlates with increased tumor aggressiveness and poor patient prognosis, making it a promising target for immunotherapy. This evidence concerns the gene PVR and neoplasm.