Moreover, surface NCL, which is anchored in the plasma membrane of hepatoma cells, interacts with the hepatoma-derived growth factor and activates pro-oncogenic PI3K/Akt pathway leading to liver carcinogenesis in humans, while blocked access to membrane NCL impairs activity of this pathway and reduces the oncogenic potential of hepatoma cells (Chen et al. 2015). The gene discussed is NUCLEOLIN; the disease is digestive system neoplasm.