The increase in phosphorylation of AS160 and AKT by insulin in the tunicamycin-treated Huh-7 cells failed to increase the uptake of glucose as seen in the vehicle treated cells (Figure 1B), suggesting that AS160 and AKT phosphorylation may not be directly involved in the tunicamycin-induced insulin resistance. The gene discussed is AKT1; the disease is Insulin resistance.