In this study, the C-terminal basic domain of SEMA3A was replaced with the heparin-binding domain (HBD) of VEGF165, hypothesizing that the resultant chimeric protein SEMA-PSI-IG-HBD would enhance antiangiogenic efficacy by: (1) competing with VEGF for NRPs (2) utilizing the HBD as a molecular anchor to increase the residence time and local concentration of the hybrid within the tumor microenvironment. This evidence concerns the gene VEGFA and neoplasm.