AKT1 and neoplasm: It was shown that the elevated levels of acetyl-CoA induced by adenosine triphosphate (ATP)-citrate lyase (ACLY) in KRAS-mutant acinar cells promoted ADM and tumor formation via histone acetylation and the mevalonate pathway.137 Fueled by the phosphorylation of acyl-CoA thioesterase (ACOT) at S392 by AKT, the accumulation of ACOT catalyzes the hydrolysis of acyl-CoA thioesters and produces nonesterified FAs and coenzyme A (CoA), which provides excessive CoA to promote the proliferation and tumor formation of PDAC cells.138