Such functional shift from E-cadherin- and LB integrin-mediated cell-cell contact to α5β1 integrin-mediated cell-ECM (i.e., fibronectin) interaction may also explain why there is elevated activation of small GTPase RhoA in CD151-deficient carcinoma cells recently described by Johnson et al [12, 29]. This evidence concerns the gene FN1 and carcinoma.