The anti-tumor activity of GYII and its decomposed recipes is, at least partly, associated with decreased heparanase and growth factor expression, which subsequently suppressed the activation of the ERK and AKT pathways, given that HS in ECM serves as a substrate of heparanase and acts in concert with growth factors such as FGF-2 and VEGF to promote tumor growth and metastasis. Here, AKT1 is linked to neoplasm.