Based on these considerations, it is possible that Th17 cells, induced by IL-23, release IL-17, which can be implicated in molecular processes leading to vascular lesions, fibrosis, and autoimmunity in patients with SSc, exploiting the binding with the IL-17 receptor expressed on fibroblasts and endothelial cells [81]. The gene discussed is IL23A; the disease is systemic sclerosis.