Thus, the expression pattern, regulatory mechanism, and αβ T cell inhibiting effect of BTN3A1 make it highly similar to PD‐L1,[57] further elaborating the notion that BTN3A1 expressed by tumor cells may be another immune checkpoint molecule rather than merely activate Vγ9Vδ2 T cells with BTN2A1 in CC. The gene discussed is BTN2A1; the disease is neoplasm.