Of note, our Her2/VEGFR2/CD3 tsAb obtained after structural optimization has strong T-cell-redirecting cytotoxic activity in vitro and in vivo against Her2- and/or VEGFR2-positive cells and overcomes the poor targeted avidity of the corresponding bsAb candidates, particularly tumor cells resistant to the combination of Herceptin and Cyramza, which suggests promising clinical application in patients with a poor prognosis due to tumor relapse or resistance to conventional antibody therapy. The gene discussed is ERBB2; the disease is neoplasm.