We have previously shown that the transgenic overexpression in mice of GDNF, a neurotrophic factor that is also involved in enteric neuronal development, is protective against HFD-induced hepatic steatosis and that hepatocytes from HFD-fed GDNF transgenic (GDNF Tg) mice have higher mitochondrial β-oxidation rates than HFD-fed control (CNTRL) mice16–18. The gene discussed is GDNF; the disease is fatty liver disease.