Animal models and clinical studies have shown that the inhibition of key enzymes of FA synthesis or beta-oxidation, such as acetyl-CoA carboxylase, acetyl-CoA synthetase, ATP citrate lyase and carnitinepalmitoyl transferase 1C, could inhibit the growth of tumour cells and delay disease progression (7–11), suggesting that FA metabolism is necessary for tumour growth and proliferation and plays an important role in tumour development. The gene discussed is ACLY; the disease is neoplasm.