The increased nuclear localisation of Smad2/3 in IPF-derived HLMFs in association with increased αSMA actin and KCa3.1 expression, and the parallel reductions in Smad2/3 nuclear localisation and αSMA expression following KCa3.1 blockade, suggest that Smad2/3 signalling is likely to be increased constitutively in IPF-derived cells. This evidence concerns the gene SMAD2 and idiopathic pulmonary fibrosis.