In particular, the incubation with SSc-ICs modulated several molecules involved in the three cardinal scleroderma pathophysiologic processes: vascular dysfunction (ET-1 and IL-8), inflammation (ICAM-1, IL-6, IFNs and MCP-1) and fibrosis (TGF-β1 and Pro-CollagenIα1). The gene discussed is TGFB1; the disease is systemic sclerosis.