Similarly, while intra-tumoral depletion of Treg cells was recently found to contribute to the anti-tumor activity of CTLA-4 mAbs in mouse models [42], intra-tumoral and splenic Treg populations were not significantly depleted by TNFR2 mAbs, and the hamster anti-TNFR2 mAbs used here did not bind detectably to mouse FcγRI or FcγRIV, indicating these mAbs are unlikely to induce ADCP (Supplementary Table S1). This evidence concerns the gene CTLA4 and neoplasm.