In the NK-cell compartment, for example, T cell immunoreceptor with Ig and ITIM domains (TIGIT) can associate with reduced cytotoxicity in some cancers, yet in glioblastoma, TIGIT+ NK cells can remain hyperfunctional or act through decoy-like mechanisms, underscoring that TIGIT biology depends on ligand availability and the surrounding cytokine milieu. This evidence concerns the gene TIGIT and glioblastoma.