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T cell-redirecting bispecific antibodies (BsAbs) are emerging as a potent cancer therapy that crosslinks tumor cells and T cells by simultaneously binding to tumor-associated antigen and CD3ε. However, immune inhibitory molecules can be remarkably upregulated after BsAbs treatment, leading to a suppressive tumor microenvironment and treatment resistance. This can be partially reversed by combination with immune checkpoint inhibitors. In our previous work, we successfully constructed the recombinant protein iRGD-antiCD3 and demonstrated