Consistent with its ability to suppress pro-fibrotic activity in myofibroblasts, and structural changes within animal models of fibrosis, the selective KCa3.1 blocker senicapoc (100 nM [10x the Kd for channel block]) significantly attenuated the TGFβ1-dependent upregulation of pivotal genes implicated in the development of IPF (n = 11 donors)(Fig. 4A and B). The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.