FAS and metabolic dysfunction-associated steatohepatitis: It has been reported that inhibition of SREBP1c mediated lipogenesis and activation of PPAR‐mediated oxidation of free fatty acids are two principal molecular targets in the treatment of nonalcoholic steatohepatitis (Musso, Cassader, & Gambino, 2016), because SREBP1c is known to play a vital role in hepatic accumulation of TG and is a major regulator of genes involving lipogenesis in the liver such as ACC and FAS (Shimano, 2009).