CXCR3 and neoplasm: We recently showed in CXCR3 knock-out mice that CD3 bsAb antitumor activity in an immunologically “cold” tumor model was dependent on the influx of T cells (15, 19–22), supporting comparable preclinical findings that higher intratumoral T-cell numbers, either present at baseline or through therapy-induced influx, improve CD3 bsAb outcomes (20, 23).