Although they demonstrated that apigenin had a higher binding affinity for IKKα than IKKβ in PC3 cells (although affinity was not quantified), they concluded that the reduction in prostate cancer growth in vitro and in vivo was a consequence of the suppression of NF-κB/p65 activation via inhibition of both isoforms, suggesting that apigenin is not a selective IKKα inhibitor in cells. Here, NFKB1 is linked to prostate cancer.