Conversely, the ubiquitin-editing enzyme A20, which is a key inflammatory and autoimmunity factor whose expression correlates with tumor aggressiveness, stabilizes Snail by mono-ubiquitination of specific Snail1 lysine residues, a mechanism that inhibits GSK3β-mediated Snail1 phosphorylation; as a result, A20 facilitates TGFβ-induced EMT in breast cancers [77]. This evidence concerns the gene SNAI1 and neoplasm.