These genetic data further question the relevance of CTLA-4 blockade in both tumor rejection and local Treg depletion and dispute the prevailing hypothesis that anti-CTLA-4 mAb induces cancer immunity through blocking the B7-CTLA-4 interaction.4 Since the therapeutic antibodies were all efficient in Treg depletion but varied in their ability to block the B7-CTLA-4 interaction, we hypothesized that these antibodies caused tumor rejection by inducing Treg depletion through antibody-dependent cellular cytotoxicity (ADCC). Here, CTLA4 is linked to cancer.