Several factors have been described, which may contribute to pDC recruitment into tumors: (i) tumor cells are capable to hijack the CXCL12/CXCR4 axis by producing SDF-1 (9, 46, 69); (ii) pDC maturation in the tumor increases CCR7 or CXCR3 levels and allows these receptors to engage with the migration machinery upon binding to CCL19/CCL21 and CXCL9/CXCL10, respectively (42–44); (iii) Maturation is induced e.g., by extracellular self-DNA bound to HMGB1 protein that prevents its degradation and is recognized by pDCs as TLR ligand (47). The gene discussed is CXCR3; the disease is neoplasm.