Overall, while the SNU398 glucagon/GCGR mechanism remains an outstanding question, due to the phenotype being observed from unrealistic levels of GCGR, a lack of signaling and growth effect robustness between cell lines, and the failure to fully restore gluconeogenic gene expression with glucagon and epigenetic inhibition, we conclude that glucagon and GCGR are not critical players in liver cancer biology. Here, GCG is linked to liver cancer.