Tregs are recruited to the tumor microenvironment via interactions between tumor-secreted chemokines and their receptors (mainly CCL17/CCL22-CCR4, CCL5-CCR5, CCL28-CCR10 and CXCL9/10/11-CXCR3), converted to a suppressive phenotype by TGF-β, and efficiently expanded in the presence of tumor-derived IL-10 and TGF-β [16]. The gene discussed is CXCR3; the disease is neoplasm.