The combination with a costimulatory αCD28 bsAb that lacks T cell-activating activity has the advantage that such an approach would allow to reduce the effective dose of the stimulatory αVEGFR2– αCD3ε bsAb and increase the selectivity for those tumor endothelial cells overexpressing VEGFR2 and TIE2, or VEGFR2 and PD-L1, respectively. This evidence concerns the gene TEK and neoplasm.