Importantly, in two murine models of PDF exposure, treatment with a neutralizing anti-IL-17A antibody inhibited peritoneal fibrosis; decreased the number of α-SMA expressing cells; and diminished the production of profibrotic factors such as TGF-β1, CTGF, and PAI-1 as well as extracellular matrix components, such as collagens and fibronectin [29,35]. The gene discussed is ACTA1; the disease is Peritoneal Fibrosis.