The single nucleotide polymorphism rs1058402G>A, causing a mutation from Ala to Thr at residue 67 of CD155, increased the binding affinity of CD155 for CD226 and generated stronger tumor immunosuppressive responses, inhibiting small‐cell lung cancer development.[63] However, in our study, the L47I, L108I, L142I, M110I, V115I, Y121A, and D117A mutations had no effect on CD155's function in glioma, suggesting that alterations at these sites mainly interfere with B7‐specific binding rather than with receptor basal activity. Here, CD226 is linked to glioma.