The increase in circulating adiponectin was associated with the activation of a set of hepatic signaling pathways mediated through AMP-activated protein kinase (AMPK), PPARα, and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), which, in turn, led to increased rates of fatty acid oxidation, prevention of hepatic steatosis, and attenuation of liver enzyme changes [9]. The gene discussed is PPARGC1A; the disease is fatty liver disease.