SNAI1 and cancer: The high plasticity of these changes requires cancer cells to switch between gene expression programs driven by multiple ligand-receptor interactions (such as TGF-β-TGFR-SMAD [16], Wnt-Frizzled-β-catenin [17] and Jag-Notch [18]) that transmit intracellular signals leading to stimulation of EMT transcription factors’ (EMT-TFs) of the SNAI1 (Snail), TWIST (Twist) and ZEB families and other TFs such as NF-κB and SMAD [15,19].