We first hypothesized that genetic alteration of HS secreted by the lymphatic endothelium might disrupt the presentation of soluble CCL21 to CCR7 receptor (with altered downstream migration signaling) on the surface of metastasizing tumor cells, a phenomenon reminiscent of the ability of sulfated domains on HS to critically "cluster" heparin-binding chemokines (e.g., as in oligomerization of IL-8 or CCL2) for receptor presentation [32]. This evidence concerns the gene CXCL8 and neoplasm.