Recent studies have provided evidence that FAP is responsible for FGF21 cleavage and inactivation, in which selective chemical inhibitors, immune depletion or genetic deletion of Fap all stabilize recombinant human FGF21 in serum [37,38]; therefore, FAP may play an important role in metabolic regulation and tumor progression by rendering the FGF21 protein inactive. The gene discussed is FGF21; the disease is neoplasm.