TIGIT and neoplasm: Our genetically modified NK cells recognize and bind CD155 via a TIGIT extracellular ligand, the binding of which to CD155 not only blocks immunosuppressive TIGIT/CD155 interactions, but also promotes GAL4-VP64 transcription factor-mediated binding to an upstream activating sequence within the construct, to spur the translation and release of an anti-CD73 scFv directly within the GBM tumor microenvironment (TME).