Taken together, AnK-treated mice had increased hepatic expression of PPARα protein to enhance fatty acids oxidation but decreased FAS protein to inhibit fatty acids synthesis coincident with suppressed SREBP1c, aP2, DGAT2, and apo CIII mRNAs, thus contributing to the hepatic triglyceride output and leading to decreased plasma triglycerides, hepatic steatosis, and total cholesterol levels. The gene discussed is ANK1; the disease is Hepatic steatosis.