Possible molecular mechanisms underlying these effects include the following: (1) HPSE degrades HS, thereby abolishing its functions as an extracellular matrix barrier; (2) Cytokines that are bound by HS, such as FGF and VEGF, are released, thereby promoting tumor cell invasion and metastasis; and (3) Biologically active, HPSE-digested HS fragments create a microenvironment that promotes tumor cell survival [8, 42, 43]. Here, VEGFA is linked to neoplasm.