The aim of this study was to determine the role of focal adhesion kinase (FAK) in the phenotypic shift between fibroblasts and myofibroblasts, two cell types important in wound healing. Signals from transforming growth factor beta (TGF) and fibronectin induce fibroblasts to differentiate into smooth muscle-actin (SMA)-expressing myofibroblasts, whereas fibroblast growth factor and heparin (FGF/h) induce myofibroblasts to loose SM expression and dedifferentiate into fibroblasts. Because we found that FAK was not necessary for TGF-mediated myofibroblast differentiation, but FAK was necessary for FGF/h-mediated inhibition of myofibroblast differentiation, we embarked on the elucidation of the role of FAK role in FGF signaling.