In light of the above, we hypothesised that healthy lung parenchyma obtained from lung resection specimens stimulated with TGFβ1 ex-vivo, would recapitulate proximal TGFβ1-dependent pro-fibrotic events evident in IPF lungs, and that these would be inhibited by the selective KCa3.1 blocker senicapoc, but not dexamethasone. Here, KCNN4 is linked to idiopathic pulmonary fibrosis.