Later, we also showed that chronically raising blood-borne ST6Gal-1 activity by subcutaneous implantation of a B16 melanoma engineered to overexpress the secretory form of the enzyme was effective in diminishing production of new granulocytes by blunting the transition of GMP to GP in granulopoiesis, and this approach was effective in controlling sterile agent-induced inflammation (1). This evidence concerns the gene ST6GAL1 and melanoma.