Indeed, XH could ameliorate hepatic steatosis and lipogenesis adipose tissue-independent mechanism that involves decreasing apolipoprotein B (apo B) secretion, downregulating/inhibiting SRREBP1/2, activating the farnesoid X receptor (FXR), suppressing diacylglycerol acyltransferase (DGAT) activity, increasing the fecal release of fats, and antioxidant-mediated suppression of LDL-c oxidation [18,25,60,78]. The gene discussed is DGAT1; the disease is Hepatic steatosis.