According to the evidence in SSc pathogenesis highlighting the contribution of Ang II and ET1 and their interaction with AT1R and ETAR via immunopathological pathways such as harmful vasoconstriction as well as pro-inflammatory and proliferative fibrosis, it is assumed that agonistic Abs targeting these vascular receptors could contribute to the pathogenesis of SSc (9). This evidence concerns the gene AGT and systemic sclerosis.