CD155 is overexpressed in tumors and involved in tumor immune escape by binding to receptors such as CD226, CD96, and TIGIT, thereby influencing the behavior of immune cells, including NK cells.[48, 49, 50] Under CD155 overexpression, these cytokine secretions regulated by B7 were significantly reduced (Figure 5B–F, all P < 0.05 vs corresponding vehicle). This evidence concerns the gene CD96 and neoplasm.