At the molecular level, AA altered the VEGF/VEGFR2 signaling pathway by inhibiting VEGF expression and VEGFR2 phosphorylation, which led to the down-regulation of the Src/FAK/ERK1/2 downstream; subsequently, the compound induced tumor anti-angiogenic effects and inhibited vascular permeability thus preventing breast cancer growth and metastasis (Figure 5). The gene discussed is VEGFA; the disease is breast carcinoma.