Since a large fraction of PTP4A1 is kept in a reduced state in the resting NHDFs and other cell types (our unpublished data and ref. 37) and we observed consistent reduction of oxo-PTP4A1-SRC complex levels after attenuation of endogenous ROS production in SScDFs, we conclude that oxidative stress is at least in part responsible for oxo-PTP4A1-SRC complex formation in SScDFs and SSc fibrotic skin and the subsequent SRC-mediated promotion of TGF-β signaling. This evidence concerns the gene PTP4A1 and systemic sclerosis.