It could inhibit the tumor migratory potential both in vivo and in vitro by reducing matrix metalloproteinases production, blocking the colony formation, decrease the mitochondrial ATP generation, suppress the beta-catenin/T-cell factor signaling and inhibit IKKβ/NF-κB signaling, independent of its hydroxylase activity [48–50]. The gene discussed is CTNNB1; the disease is neoplasm.