Overall, in combination with the results of Fig. 5, Fig. 6, these data strongly demonstrate that High BCAA feeding is both sufficient to inhibit hepatic lipid synthesis via inhibition of AHR/MAPK9 mediated DNL and activating PPAR-RXR mediated fatty acid β-oxidation, which is necessary for a High BCAA diet to maximally ameliorate hepatic steatosis. The gene discussed is MAPK9; the disease is fatty liver disease.