Recent evidences have indicated that stiffness of extracellular matrix (ECM) works as crucial cues to control cell behaviors, including cyst- and tubule-formation of epithelial cells. Although cell-ECM adhesion sites, called focal adhesions, are thought to play a critical role in sensing ECM stiffness, molecular mechanisms underlying this process are largely unknown. We have shown that the interaction of vinculin and vinexin, both of which are adaptor-type focal adhesion proteins, works as a "mechanosensor" for ECM stiffness and regulates stiffness-dependent cell migration of fibroblast cells. We have also found that one of vinexin paralog, CAP, has similar function to vinexin, but another paralog, ArgBP2 does not, suggesting the diverse function of vinexin family proteins. Furthermore, in order to clarify the mechanism by which ECM stiffness regulates the cyst- and tubule-formation of epithelial cells, we established the mammary epithelial cells in which vinculin gene is disrupted using CRISPR/Cas system. Vinculin functions in cyst formation of mammary epithelial cells will be examined using these cells.