For instance, Pohl and colleagues showed that the restoration of expression of SMAD4 (the binding partner of SMAD3 required in order for SMAD3 to enter the nucleus and activate its target genes) in SW480 colon carcinoma cells led to reversion from a mesenchymal-like phenotype to an epithelial-like phenotype [34]. This evidence concerns the gene SMAD4 and colon carcinoma.