In contrast, on the cancer cell side, PVR interaction with ligands TIGIT or DNAM leads to tyrosine phosphorylation of the PVR’s ITIM domain by Src kinases and recruitment of SHP-2 followed by dephosphorylation of focal adhesion kinase and paxillin thereby reducing adhesion, increasing motility, survival, and proliferation of cancer cells.283–285 Therefore, it is conceivable that if exhausted NK cells cannot kill cancer cells, they could make them stronger through stimulation of PVR or other immune checkpoints, especially with the ability of some NK cell subsets to support angiogenesis.286. The gene discussed is PXN; the disease is cancer.