Evidence from our previous studies suggests that TNBC cells secrete IL-6, which interacts with the IL-6 receptor on tumor-associated lymphatic vessels in the tumor microenvironment or on lymphatic vessels in distant organs and that the activated IL-6 receptor stimulates the STAT3 signaling pathway, which results in upregulated CCL5 expression and secretion by LECs. The gene discussed is CCL5; the disease is neoplasm.