We have previously shown that PRA coexpression potentiated PRB-mediated cancer cell migration and that PR isoforms differentially regulated expression of major players of cell migration [41] such as urokinase plasminogen activator (uPA), its inhibitor plasminogen activator inhibitor type 1 (PAI-1), uPA receptor (uPAR), and β1-integrin, which affect focal adhesion kinase (FAK) signaling. This evidence concerns the gene PTK2 and cancer.