In prostate and melanoma cancer models, the inhibition of Cdk5 resulted in decreased cell motility and metastatic potential [9,12] and in breast cancer, Cdk5 controlled cancer cell migration and tumor formation by regulating the phosphorylation of focal adhesion kinase (FAK) at Ser-732, as a downstream step of transforming growth factor Beta (TGF-B1) signaling, and was shown to be essential for epithelial to mesenchymal transition (EMT) and cell motility [10]. This evidence concerns the gene CDK5 and breast carcinoma.