The treatmentshifted mitochondrial dynamics toward mitochondrial fusion by up-regulatingthe expression of Mfn2, and it exhibited antimetastatic activity byup-regulating the expression of metallopeptidase inhibitor 3 (Timp-3)and decreasing hepatic matrix metallopeptidase 9 (MMP9) content.63 Another potential therapeutic target for canceris the C–C motif chemokine ligand 2 (CCL2), which is overexpressedin cancer cells. The gene discussed is MMP9; the disease is cancer.