Humoral factors, such as interleukin-6, macrophage colony-stimulating factor, and receptor activator of NF-kappaB ligand, seem to promote osteoclastogenesis and the survival of osteoclasts.[6,7,11] Furthermore, the augmented number of macrophage-like cells in GSD lesions produce VEGF-A, VEGF-C, and VEGF-D that can stimulate differentiation into osteoclasts and lymphangiogenesis.[12] Conversely, some studies have suggested that bone resorption may be secondary to lymphangiogenesis. Here, IL6 is linked to disorder of glycogen metabolism.