Supporting this, some researchers have observed that NK cells with high expression of TIGIT have a low cytotoxic capacity, mainly due to their greater affinity for CD155 and that the TIGIT/CD155 binding avoids interaction with the activating receptor CD226 and prevents its homodimerization [68, 69]; thus, the use of a monoclonal antibody against TIGIT could avoid the interaction with this inhibitory ligand and improve the response against these tumor cells. This evidence concerns the gene CD226 and neoplasm.