Significantly, recent experiments from our laboratories have demonstrated that the FAK homolog Proline-Rich Tyrosine Kinase 2 (Pyk2) is upregulated in bladder cancer tissues compared to normal tissue controls and plays a more important role than FAK in regulating IGF-I-induced motility and invasion of urothelial carcinoma cells [37]. This evidence concerns the gene IGF1 and urinary bladder carcinoma.