The results suggest that by supporting insulin/IGF signaling networks with the appropriate classes of PPAR agonists, the severity of hepatic steatosis and abundance of mega-mitochondria decline, and the cascade leading to liver degeneration, including ER stress (manifested by disruption of the tubular architecture), mitochondrial dysfunction (mega-mitochondria), and fibrogenesis (increased Sirius red staining of sinusoidal and peri-hepatocyte collagen) can be curtailed or interrupted. The gene discussed is IGF1; the disease is fatty liver disease.