Despite little being known about the mechanism by which cancer cells enter and maintain a dormant state, and what triggers the resumption of aggressive growth, the interaction of cells with the extracellular matrix environment (with particular reported roles for Type I collagen, fibronectin and integrins and subsequent activation of FAK [44, 45]) appears to facilitate re-entry to the metastatic phenotype [46, 47]. This evidence concerns the gene PTK2 and cancer.