Accordingly, a bi-specific antibody generated by genetic fusion of the C-terminus of the anti-VEGF-A antibody Bevacizumab with a peptide that specifically binds to the VEGF-binding pocket in NRP1 b1 domain [119], inhibits EC migration induced by pro-angiogenic factors and has a more potent anti-tumour activity than Bevacizumab in a murine tumour xenograft model [120]. The gene discussed is NRP1; the disease is neoplasm.