Given the fact that NK cells are deactivated via hTIGIT interaction to PVR57, but also via interaction with the low-affinity receptor Nectin-2, both of them strongly expressed on the surface of cancer cells58, we conclude that the Fap2 affinity to hTIGIT is sufficient for NK cell deactivation, independent of cancer cell receptor binding to hTIGIT. Here, NECTIN2 is linked to cancer.