The knockdown of RNase L increased prostate cancer cell migration [54] and enhanced tumor growth and metastasis following implantation in the mouse prostate [55], the mechanism of which was related with an increased cell surface expression of integrin β1 and activation of the focal adhesion kinase-sarcoma pathway and the Ras-related C3 botulinum toxin substrate 1-guanosine triphosphatase activity [54]. The gene discussed is RAC1; the disease is prostate cancer.