As expected, the ablation of CD3 binding abolished the HER2-mCD3-Fc bsAb’s ability to trigger human T-cell-dependent cytotoxicity (Figure 5I,J) and IFN-λ/granzyme B secretion (Figure 5K–P) against the HER2-overexpressing tumor cells, suggesting that the HER2-CD3-Fc bsAb relies on CD3 binding to recruit T cells and elicit antitumor activity. The gene discussed is GZMB; the disease is neoplasm.