It has been previously shown that depletion of FAP-α-expressing stromal cells can impair the growth of immunogenic tumours via a lymphocyte dependent mechanism and that inhibition of FAP-α using extracellular competitive inhibitors of dipeptidyl peptidases have been shown to contribute to impaired epithelial cancer growth via a FAP-α dependant mechanism[36-39]. The gene discussed is FAP; the disease is neoplasm.