Interestingly, BTN3A1-induced immunosuppression was reported for BTN3A1 overexpressing tumor cells, and it is abolished by BTN3A1-V domain-specific mAbs and by Zoledronate53 It will be interesting to learn whether V-domain interactions between constitutively expressed BTN2A1 and BTN3A13,57 or newly formed PAg-induced BTN3A-BTN2A1 complexes13,20,35,59 might affect such suppression. Here, BTN2A1 is linked to neoplasm.