In summary, the data presented demonstrate that apigenin intake in a mouse model of prostate cancer can suppress NF-κB activation, and its DNA binding reduces the expression of downstream target proteins COX-2, VEGF, cyclin D1, Bcl2 and Bcl-xL resulting in cell cycle arrest and induction of apoptosis in prostate tumors. The gene discussed is NFKB1; the disease is prostate carcinoma.