Our peptide designing strategy based on the receptor-binding segments of VEGF-B and VEGF-A led to the abrogation of the angiogenesis signaling factors, i.e. VEGFR1 and -R2, AKT and ERK1/2, followed by a notable decrease in tumor cell proliferation (Ki67 expression) and angiogenesis (expression of CD31 and CD34), and also caused promotion of apoptosis (increased TUNEL staining and P53 expression and decreased Bcl-2 expression) and a significant decrease in metastasis-related factors (increased E-cadherin and decreased N-cadherin, NF-κB and MMP-9 expression). The gene discussed is AKT1; the disease is neoplasm.