We can hypothesize that high level of circulating BTN2A1 could lead to Vγ9Vδ2 T-cells exhaustion that facilitate tumor immune escape mechanisms (18), and/or activate Vγ9Vδ2 T cells with pro-tumorigenic characteristics, and explain the poorer outcomes of patients with high level of circulating BTN2A1. The gene discussed is BTN2A1; the disease is neoplasm.