Anti-AT1R and anti-ETAR autoantibodies directly induce collagen production by skin fibroblasts (134) and regulate the synthesis of profibrotic factors such as transforming growth factor β (TGF-β) by human dermal microvascular endothelial cells (130), which are pathological mechanisms in SSc patients who develop lung fibrosis. This evidence concerns the gene AGTR1 and pulmonary fibrosis.