Present results, combined with our earlier report of pro-migratory functions of VEGF-C [27], and reported VEGF-C mediated stimulation of CCL21 secretion by LECs [21], endorses the idea that the interplay/crosstalk between CCL21 chemokine and VEGF-C promotes breast cancer progression through several distinct, but complementary mechanisms. The gene discussed is CCL21; the disease is breast cancer.