Alarge and growing literature supports the involvement of protein tyrosine kinases in the regulation of vascular cell behavior. Many growth factor receptors are tyrosine kinases, and many cytosolic signaling events are regulated by protein tyrosine phosphorylation. Many of these mitogens, receptors, and intracellular kinases have been studied in vivo in various vascular injury and remodeling models. The biochemical counterpoint to these phosphorylation steps, ie, the reverse reaction of dephosphorylation, has received much less attention in vascular injury studies. This deficiency has begun to be addressed by the rigorous report of Wright et al in this issue.1 These authors have examined the expression in the artery wall of a family of enzymes, the protein tyrosine phosphatases (PTPases), which dephosphorylate phosphorylated tyrosine residues.