Increased expression and activity of KCa3.1 channels is found in IPF-derived human lung myofibroblasts, and inhibition of the channel through selective inhibitors attenuates pro-fibrotic behaviour in these cells, including proliferation, differentiation, wound healing, collagen secretion, contractility and α-smooth muscle actin expression in response to TGF-β124–26. The gene discussed is KCNN4; the disease is idiopathic pulmonary fibrosis.