In hepatocellular carcinoma (HCC), CCRK mediates tumor development in different etiologies, including hepatitis B virus infection [131], non-alcoholic fatty liver disease [132], via orchestrating a self-reinforcing circuitry comprising of AR, GSK3β, β-catenin, AKT, EZH2, and NF-κB signaling, and also facilitate tumor immune evasion [133,134,135]. This evidence concerns the gene GSK3B and hepatocellular carcinoma.