Consistent with the results in 2-AG-treated HepG2 cells, GN treatment reversed tunicamycin-induced expression of gluconeogenesis genes including CREBH, PEPCK, and G6Pase. Taken together, these results indicate that GN inhibits CB1R-induced gluconeogenesis via suppression of ER stress, which might contribute to improvement of hyperglycemia. The gene discussed is CNR1; the disease is Hyperglycemia.