Current studies on the mechanisms by which LHB with pre-S mutations accelerates the progression of the cell cycle in HCC include investigations of direct binding to JAB1 (Jun activation domain binding protein 1), which leads to degradation of the oncogene p27, cyclin A upregulation, and induction of hepatocyte nodal proliferation through an ER stress-independent mechanism [31,32]. The gene discussed is COPS5; the disease is hepatocellular carcinoma.