If KCa3.1 is expressed in primary HBEC, it is therefore unclear whether its inhibition might be deleterious in asthma through the inhibition of epithelial cell wound healing, proliferation, airway lining fluid secretion and ciliary beat, or beneficial though the inhibition of chemokine/cytokine production, mucus secretion and epithelial mesenchymal transition (EMT). This evidence concerns the gene KCNN4 and asthma.