We previously described the anti-fibrotic effects of the KCa3.1 ion channel in our ex vivo human lung model of fibrogenesis and showed significant inhibition of 28 TGFβ1-dependent genes including many molecules implicated in IPF pathophysiology, as well as reduced tissue fibroblast numbers, αSMA protein expression and tissue type I and III collagen expression. The gene discussed is ACTA1; the disease is idiopathic pulmonary fibrosis.