Interestingly, in the absence of PAM, when the γ9δ2TCR interaction with its ligands BTN2A1 and BTN3A is suboptimal, the combination of D24-RGD with TEGs resulted in a significant increase in tumor killing from approximately 13% to 30% for SU-DIPG-IV cells (Figure 2G), whereas the combination with R124 increased the killing of VUMC-DIPG-G cells from 16% to 40% (Figure 2H). The gene discussed is BTN2A1; the disease is neoplasm.