Increased interactions between cancer cells and the ECM can therefore alter the mechanical response of cells through an interlinked hub of mechanochemical systems, including adhesion receptors like integrins, intracellular focal adhesions like talin-1, vinculin, focal adhesion kinase (FAK) and Crk-associated substrate (p130Cas or synonymously referred to as breast cancer anti-estrogen resistance 1 (BCAR1)), cytoskeletal networks such as actin, microtubules, and intermediate filaments, and molecular motors like myosin [17,81]. This evidence concerns the gene PTK2 and cancer.