They also provided evidence that Ex-4 independently increased the phosphorylation of 3-phosphoinositide-dependent kinase-1 (PDK-1), protein kinase B (AKT) and protein kinase C (PKC-ζ) in HepG2 and HuH-7 cells, reducing their triglyceride stores and, consequently, hepatocyte steatosis, providing a plausible mechanism by which Ex-4 bypasses AKT activation in patients with hepatic insulin resistance. The gene discussed is AKT1; the disease is steatosis.