SNAI1 and cancer: Increased Src activity drives EMT by inducing: i) cytoplasmic accumulation of β-catenin leading to dissociation of cell-cell junctions [27]; ii) β-catenin transcriptional activity that in turn promotes EMT through Snail1 over-expression; iii) tyrosine phosphorylation of cortactin leading to cytoskeleton activation and cell motility [28]; and iv) activation of Twist, that promotes the generation of an aggressive cancer stem cell phenotype [29].