In accordance with this finding, the knockdown of p65 by p65 siRNA effectively attenuated the EYA4 depletion-mediated up-regulation of RAP1 protein expression in HCC cells (Fig. 4i), implying a critical role for NF-κB in the EYA4-dependent repression of RAP1 transactivation. The gene discussed is RAP1A; the disease is hepatocellular carcinoma.