Critically, CRISPR/Cas9-mediated ablation of BTN2A1 did not impair the suppressive potential of BTN3A1 against αβ T cells in the setting of ovarian cancer [17], suggesting that the particular dynamics of BTN3A1:BT2A1 interactions can dictate either the activation of Vγ9Vδ2 T cells, or the suppression of αβ T cells. The gene discussed is BTN3A1; the disease is ovarian cancer.