As shown by in vitro investigations, excessive collagen production by skin fibroblasts or increased release of reactive oxygen species (ROS) by neutrophils is induced by Abs against AT1R and ETAR, which are involved in mechanisms that contribute to progressive fibrosis of the skin and lungs as well as vasculopathy, resulting in organ dysfunction and failure (7, 83). This evidence concerns the gene AGTR1 and vascular disorder.