In vivo, the activity of DPP4 is strongly correlated with N-terminal CXCL10 processing, and directly limits the migration of CXCR3+ lymphocytes to melanoma tumour tissues [15]; accordingly, inhibition of DPP4 enhances tumour suppression in this model through the preservation of biologically active, agonistic CXCL10. The gene discussed is CXCR3; the disease is neoplasm.