“…Once activated by integrins, G protein-coupled receptor ligands, or growth factors and neuromediators, FAK is autophosphorylated at tyrosine 397 (Y397), then binds and activates downstream proteins such as Src, p130CAS, paxillin, and PI3KR2 [7,8,9], finally leading to cell adhesion, migration, invasion, survival, proliferation, angiogenesis, immune suppression, and regulation of DNA damage repair [8,9,10,11]. Because of these roles and its overexpression in many cancers, with the correlation to poor prognosis in some of them [12,13,14,15,16,17,18,19,20,21,22,23], FAK is believed to play a role in cancer development and progression. Small-molecule inhibitors targeting the FAK kinase domain (e.g., PF-573,228) have, therefore, been developed as potential anti-cancer targeted therapies.…”