TIGIT, which normally binds CD155 and CD112 on DCs and tumour cells, exerts its immunosuppressive function through numerous mechanisms, such as its direct binding to tumour expressing CD155 to trigger T/NK cell inhibition, outcompeting its co-stimulatory counterpart, CD226 on the T/NK cell surface and by indirect means including the activation of immunosuppressive DCs and Tregs following CD155-CD226 recognition [267]. Here, CD226 is linked to neoplasm.