Since, in prostate cancer cells, the antitumor effect of apigenin was reported to be mediated by its ability to directly interact with IKKα and suppress NF-κB/p65 activation, we analyzed the activation of the NF-κB/p65 subunit (measured as levels of P-p65) in the three types of C57 cells. This evidence concerns the gene CHUK and prostate carcinoma.