This is an interesting result since it was described that the regulation of IKKα by apigenin occurred both in the cytoplasm and in the nucleus of PC3-tumor prostate cells [33]; moreover, in contrast to the results obtained in prostate cancer cells in which one of the main mechanisms of action of apigenin is the IKKα-mediated inhibition of the activation of NF-κB/p65, we have found that, in the C57 cells, apigenin does not inhibit the activation of this signaling pathway in a relevant way, even at high concentrations of apigenin (20–40 μM). Here, NFKB1 is linked to neoplasm.