Mechanistically, these findings were linked to the downregulation of tumor-promoting molecules, including cyclooxygenase-2 (COX-2), vascular endothelial growth factor [VEGF], and vasodilator-stimulated phosphoprotein (VASP), alongside an upregulation of AMP-activated protein kinase (AMPK) [96]. The gene discussed is VASP; the disease is neoplasm.