“… 10 , 11 , 12 Activation of HSCs is considered a crucial event that promotes increased extracellular matrix production and hepatic fibrosis, leading to the increased risk of hepatocarcinoma development. 13 It is reported that HSCs activation relies, at least partially, on a direct role of acetyl coenzyme A (CoA) carboxylase (ACC) by stimulating de novo synthesis of fatty acids. 14 Specifically, ACC1 catalyzes the rate-limiting step of de novo lipogenesis, conversion of acetyl CoA to malonyl-CoA, and an ACC inhibitor called GS-0976 is in clinical trials for the treatment of NASH.…”