Overall, the combination of Amy-F with RT robustly regulated the TGF-β signaling via the down-regulation of VEGF, INF-γ, IL-2, and IL-6 levels in treated BCCs and exhibited superior influence when compared to control, Amy-F, and RT groups, and thus abolished the pro-angiogenic and metastatic ability of human breast cancer cells. The gene discussed is TGFB1; the disease is breast cancer.