Consistent with our hypothesis that oxidative stress plays a crucial role in the development of SSc vasculopathy, ECs from SSc patients were previously reported to have the ability to produce H2O2 (Servettaz et al., 2007) which may inhibit endothelial differentiation due to a reduced octamer-binding transcription factor 4 (Oct-4) expression (Xiao et al., 2014). This evidence concerns the gene POU5F1 and systemic sclerosis.