Collectively, these data indicated that the serine/threonine phosphatase activity of EYA4 dephosphorylated IκBα, counteracted IκBα ubiquitination and degradation, blocked p65 nuclear translocation and thus inactivated NF-κB signaling, which have documented roles in the tumorigenesis of HCC cells. Here, NFKB1 is linked to hepatocellular carcinoma.