Oxidation of the active site Cys of PTPs by ROS via formation of sulfenic acid — which leads in a subset of PTPs, such as PTP4A1, to disulfide bridge formation — is a well-known mechanism for physiological and pathological downregulation of their activity (6) and has been proposed to play a role in the pathogenesis of SSc fibrosis by promoting growth factor signaling (7). The gene discussed is PTS; the disease is systemic sclerosis.