For instance, the genetic ablation of FASN, which is responsible for synthesizing palmitate (C16:0) from acetyl‐CoA and malonyl‐CoA in the presence of NADPH, completely suppresses the Akt‐driven HCC development through inhibiting the Rictor/mammalian target of rapamycin complex2 (TORC2) signalling.11 ACC, which converts acetyl‐CoA to malonyl‐CoA as the first rate‐limiting step in de novo lipogenesis, has attracted wide attention as a therapeutic target for non‐alcoholic steatohepatitis (NASH). This evidence concerns the gene FASN and metabolic dysfunction-associated steatohepatitis.