PTK2 and neoplasm: The main mechanism of FAK-mediated tumor cell tail FAs disassembly involves the following pathways [4–8]: phosphorylation of FAK recruits calpains to FAs, which degrade FAK and promote FA disassembly; FAK also regulates FA disassembly by activating RACK1, which in turn affects the activity of ERK located at FAs; and FAK interacts with the dynein Dyn2, affecting clathrin-dependent vesicle endocytosis to promote FAs disassembly.