Similar to previous reports showing that ACLY- or CRAT-deficient cancer cells displayed defective lipid synthesis and an increase in fatty acids29–31, our data showed that knocking down Acly, Acss2, or Crat perturbed lipid metabolism and led to fatty acid accumulation, indicating that metabolic imbalance likely resulted from a shortage of intracellular Ac-CoA pools. This evidence concerns the gene ACSS2 and cancer.